To Traffic-related Air Pollution Exposure Research Articles

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.

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.

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.

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.

Air pollution and high-intensity interval exercise: Implications to anti-inflammatory balance, metabolome and cardiovascular responses

High-intensity interval exercise (HIIE) is an effective non-pharmacological tool for improving physiological responses related to health. When HIIE is performed in urban centers, however, the exerciser is exposed to traffic-related air pollution (TRAP), which is associated with metabolic, anti-inflammatory imbalance and cardiovascular diseases. This paradoxical combination has the potential for conflicting health effects. Thus, the aim of this study was to determine the effects of HIIE performed in TRAP exposure on serum cytokines, non-target metabolomics and cardiovascular parameters. Fifteen participants performed HIIE in a chamber capable to deliver filtered air (FA condition) or non-filtered air (TRAP condition) from a polluted site adjacent to the exposure chamber. Non-target blood serum metabolomics, blood serum cytokines and blood pressure analyses were collected in both FA and TRAP conditions at baseline, 10 min after exercise, and 1 h after exercise. The TRAP increased IL-6 concentration by 1.7 times 1 h after exercise (p < 0.01) and did not change the anti-inflammatory balance (IL-10/TNF-α ratio). In contrast, FA led to an increase in IL-10 and IL-10/TNF-α ratio (p < 0.01), by 2.1 and 2.3 times, respectively. The enrichment analysis showed incomplete fatty acid metabolism under the TRAP condition (p < 0.05) 10 min after exercise. There was also an overactivity of ketone body metabolism (p < 0.05) at 10 min and at 1 h after exercise with TRAP. Exercise-induced acute decrease in systolic blood pressure (SBP) was not observed at 10 min and impaired at 1 h after exercise (p < 0.05). These findings reveal that TRAP potentially attenuates health benefits often related to HIIE. For instance, the anti-inflammatory balance was impaired, accompanied by accumulation of metabolites related to energy supply and reduction to exercise-induced decrease in SBP.

Dynamic molecular choreography induced by traffic exposure: A randomized, crossover trial using multi-omics profiling

The biological mechanism of adverse health outcomes related to exposure to traffic-related air pollution (TRAP) needs elucidation. We conducted a randomized, crossover trial among healthy young students in Shanghai, China. Participants wore earplugs and were randomly assigned to a 4-hour walking treatment either along a traffic-polluted road or through a traffic-free park. We conducted untargeted analyses of plasma exosome transcriptomics, serum mass spectrometry-based proteomics, and serum metabolomics to evaluate changes in genome-wide transcription, protein, and metabolite profiles in 35 randomly selected participants. Mean personal exposure levels of ultrafine particles, black carbon, nitrogen dioxide, and carbon monoxide in the road were 2–3 times higher than that in the park. We observed 3449 exosome mRNAs, 58 serum proteins, and 128 serum metabolites that were significantly associated with TRAP. The multi-omics analysis showed dozens of regulatory pathways altered in response to TRAP, such as inflammation, oxidative stress, coagulation, endothelin-1 signaling, and renin-angiotensin signaling. We found that several novel pathways activated in response to TRAP exposure: growth hormone signaling, adrenomedullin signaling, and arachidonic acid metabolism. Our study served as a demonstration and proof of concept on the evidence that associated TRAP exposure with global molecular changes based on the multi-omics level.

Association of traffic-related air pollution with Newborn's anthropometric indexes at birth

An emerging body of evidence has associated exposure to traffic-related air pollution (TRAP) during pregnancy with birth outcomes. However, the evidence on the association of TRAP exposure and 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. This cross-sectional study was based on hospital medical records of 4053 mother-neonate pairs between May 16, 2016, and December 5, 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. The median (IQR) of BW, BL, and HC of newborns were 3250 (592) gr, 51.0 (3.5) cm, 35 (2) cm, respectively. The adjusted models revealed that higher exposure to PM2.5 and PM10 was significantly related with lower BW and BL. Similar 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. Overall, our findings suggested that higher prenatal exposure to TRAP was related with lower BW, BL and HC.

Results of an HEI Systematic Review on the Health Effects of Long-term Exposure to Traffic-Related Air Pollution

BACKGROUND AND AIM: After a broad search, the HEI Panel on the Health Effects of Long–Term Exposure to Traffic–Related Air Pollution (TRAP) identified 1100 studies relevant for further screening, 352 of which met the inclusion criteria and are considered in the systematic review. Respiratory effects in children (N=117) and birth outcomes (N=86) were the most common outcomes published in the literature. Slightly fewer studies investigated cardiometabolic effects (N=57), respiratory effects in adults (N=50), and mortality (N=48). METHODS: The systematic review is undergoing independent peer-review and publication is aimed for late 2021. RESULTS:The Panel’s initial findings were for a moderate to high level of confidence in an association between exposure to TRAP with term low birth weight. They also reported a moderate or high level of confidence in an association between exposure to TRAP and asthma onset in children and adults, and occurrence of acute respiratory infections in children. Furthermore, they found moderate evidence for an association between exposure to TRAP and ischemic heart disease, stroke, and diabetes mellitus. The overall confidence in an association between TRAP exposure and mortality was high for all-cause, circulatory, ischemic heart disease mortality; moderate to high for lung cancer mortality; and moderate for respiratory mortality. For the other health outcomes assessed, the confidence was very low or low for an association with TRAP, and the evaluation was often limited by the small numbers of studies. CONCLUSIONS:In light of the large number of people exposed to TRAP – both in and beyond the near–road environment, the Panel concluded that the moderate to high confidence in an association between long-term exposure to TRAP and various adverse health effects indicates that exposures to TRAP are an important public health concern and deserve continued targeted policy and broader public focus. KEYWORDS: traffic-related air pollution, systematic review, birth outcomes, cardiometabolic effects, respiratory effects, mortality

Knowledge on adverse effects of traffic-related air pollution: have we filled the gap? What more do we need to know?

BACKGROUND AND AIM: The Health Effects Institute has conducted a systematic review on the health effects of long-term exposure to traffic-related air pollution (TRAP) and selected adverse health outcomes, with an expert Panel. The findings have provided a moderate or high level of confidence in the presence of an association between long-term exposure to TRAP and various adverse health effects. Although the evidence is already compelling for some of the outcomes investigated, a number of future research opportunities emerged from the results of this report. METHODS: Critical evaluation of research needs. RESULTS:NO2 was the TRAP exposure indicator used most often in the review. There remains a need to gain a better understanding of whether the epidemiological associations found for TRAP are due to direct effects of NO2, or to another component of TRAP, or to the broader mixture of correlated components indicative of TRAP. There is a need for additional epidemiological studies on an array of traffic pollutants including UFP and non-tailpipe PM indicators, because there were few studies and there are good reasons to suspect they might be health relevant beyond what is already known. Studies have been conducted on populations residing in a wide range of countries, though the majority were done in Europe and North America. Hence there is a need for more health studies in areas outside North America and Europe. Additional studies should evaluate the role of spatially correlated factors that may either confound and/or modify the health effects of TRAP, most notably traffic noise, and factors related to the built environment, such as presence of green space. Finally, various suggestions to improve methods in study design, analysis and evidence synthesis were identified. CONCLUSIONS:The systematic review helped to identify several important areas for future research. KEYWORDS: Systematic review, traffic-related air pollution, cardiovascular effects, respiratory effects, mortality

Early childhood traffic-related air pollution and risk of allergic rhinitis at 2\u20134 years of age modification by family stress and male gender: a case-control study in Shenyang, China

BackgroundFew studies have explored the modifications by family stress and male gender in the relationship between early exposure to traffic-related air pollution (TRAP) and allergic rhinitis (AR) risk in preschool children.MethodsWe conducted a case-control study of 388 children aged 2–4 years in Shenyang, China. These children AR were diagnosed by clinicians. By using measured concentrations from monitoring stations, we estimated the exposures of particulate matter less than 10 μm in diameter (PM10), nitrogen dioxide (NO2), ozone (O3), carbon monoxide (CO), and sulfur dioxide (SO2) in preschool children aged 2–4 years. After adjusted potential confounding factors, we used logistic regression model to evaluate the odds ratio (OR) and 95% confidence interval (CI) for childhood AR with exposure to different air pollutants according to the increasing of the interquartile range (IQR) in the exposure level.ResultsThe prevalence of AR in children aged 2–4 years (6.4%) was related to early TRAP exposure. With an IQR (20 μg/m3) increase in PM10 levels, an adjusted OR was significantly elevated by 1.70 (95% CI, 1.19 to 2.66). Also, with an IQR (18 μg/m3) increase in NO2, an elevated adjusted OR was 1.85 (95% CI, 1.52 to 3.18). Among children with family stress and boys, PM10 and NO2 were positively related to AR symptoms. No significant association was found among children without family stress and girls.ConclusionsFamily stress and male gender may increase the risk of AR in preschool children with early exposure to PM10 and NO2.

Effect of Reducing Ambient Traffic-Related Air Pollution on Blood Pressure: A Randomized Crossover Trial.

Exposure to traffic-related air pollution (TRAP) may contribute to increased prevalence of hypertension and elevated blood pressure (BP) for residents of near-highway neighborhoods. Relatively few studies have investigated the effects of reducing TRAP exposure on short-term changes in BP. We assessed whether reducing indoor TRAP concentrations by using stand-alone high-efficiency particulate arrestance (HEPA) filters and limiting infiltration through doors and windows effectively prevented acute (ie, over a span of hours) increases in BP. Using a 3-period crossover design, 77 participants were randomized to attend three 2-hour-long exposure sessions separated by 1-week washout periods. Each participant was exposed to high, medium, and low TRAP concentrations in a room near an interstate highway. Particle number concentrations, black carbon concentrations, and temperature were monitored continuously. Systolic BP (SBP), diastolic BP, and heart rate were measured every 10 minutes. Outcomes were analyzed with a linear mixed model. The primary outcome was the change in SBP from 20 minutes from the start of exposure. SBP increased with exposure duration, and the amount of increase was related to the magnitude of exposure. The mean change in SBP was 0.6 mm Hg for low exposure (mean particle number and black carbon concentrations, 2500 particles/cm3 and 149 ng/m3), 1.3 mm Hg for medium exposure (mean particle number and black carbon concentrations, 11 000 particles/cm3 and 409 ng/m3), and 2.8 mm Hg for high exposure (mean particle number and black carbon concentrations, 30 000 particles/cm3 and 826 ng/m3; linear trend P=0.019). There were no statistically significant differences in the secondary outcomes, diastolic BP, or heart rate. In conclusion, reducing indoor concentrations of TRAP was effective in preventing acute increases in SBP.

Accelerated epigenetic age as a biomarker of cardiovascular sensitivity to traffic-related air pollution.

Background: Accelerated epigenetic age has been proposed as a biomarker of increased aging, which may indicate disruptions in cellular and organ system homeostasis and thus contribute to sensitivity to environmental exposures.Methods: Using 497 participants from the CATHGEN cohort, we evaluated whether accelerated epigenetic aging increases cardiovascular sensitivity to traffic-related air pollution (TRAP) exposure. We used residential proximity to major roadways and source apportioned air pollution models as measures of TRAP exposure, and chose peripheral arterial disease (PAD) and blood pressure as outcomes based on previous associations with TRAP. We used Horvath epigenetic age acceleration (AAD) and phenotypic age acceleration (PhenoAAD) as measures of age acceleration, and adjusted all models for chronological age, race, sex, smoking, and socioeconomic status.Results: We observed significant interactions between TRAP and both AAD and PhenoAAD. Interactions indicated that increased epigenetic age acceleration elevated associations between proximity to roadways and PAD. Interactions were also observed between AAD and gasoline and diesel source apportioned PM2.5.Conclusion: Epigenetic age acceleration may be a biomarker of sensitivity to air pollution, particularly for TRAP in urban cohorts. This presents a novel means by which to understand sensitivity to air pollution and provides a molecular measure of environmental sensitivity.

Cumulative Early-Life Traffic-Related Air Pollution Exposure and Sleep Disturbance Consistent with Sleep Disordered Breathing among 12-Year-Old Children

Background/Aim: Exposure to traffic-related air pollution (TRAP) may be linked to sleep disordered breathing. The aim of this study was to assess whether cumulative early-life exposure to TRAP is associated with loud snoring and frequent napping among 12-year-old children.Methods: We used data from the Cincinnati Childhood Allergy and Air Pollution Study, a prospective birth cohort study of children in the greater Cincinnati, Ohio metropolitan area. Annual average exposures to TRAP at residential addresses from birth to 12-years-old were estimated using a previously-validated land use regression model of elemental carbon attributable to traffic. TRAP was dichotomized as high versus low at the 75th percentile (0.41 µg/m3) based on the distribution at age 12 years. Parental report of frequency of their child snoring loudly and napping was categorized as &lt;3 times per week versus ≥3 times per week. Using log-binomial regression, we estimated prevalence ratios (PR) of frequent loud snoring and napping among children with high versus low TRAP exposure. Models were adjusted for age, sex, race/ethnicity, annual household income, secondhand smoke expo-sure, and obesity status (95th body mass index percentile).Results: Among 313 children, the prevalence of frequent loud snoring was 10.0% and frequent napping was 12.0%. There was an over 2-fold higher prevalence of frequent snoring among children with high versus low TRAP exposure in the fully-adjusted model (PR:2.20, 95%Confidence Interval [CI]:1.10-4.40, p=0.025). There was over twice the prevalence of frequent napping among children with high versus low TRAP exposure in the unadjusted model (PR:2.48, 95%CI:1.38-4.46, p=0.002); however, this association was attenuated in the fully-adjusted model (PR:1.12, 95%CI:0.65-1.92, p=0.68).Conclusions: High levels of cumulative early-life TRAP exposure may contribute to symptoms consistent with sleep disordered breathing among children, which are both associated with a wide range of adverse human health effects including poor cardiometabolic health. More research is warranted.

Attributing School Air Pollution Levels to Features of the Built Environment in New York City

Background: Exposure to traffic-related air pollution (TRAP) has been linked to asthma prevalence and exacerbations. Children spend a significant portion of their day in school where exposure to pollutants can be high based on geographic features of the built environment. The study objective was to determine the distributions of geographic indicators of traffic and built environment features and the association with school-based TRAP exposure in New York City (NYC).Methods: Spatial data on the proximity and density of roadways and built environment features were examined for a 250-meter buffer around NYC elementary and middle schools (N=1184). Annual average levels of particulate matter &lt;2.5 microns (PM2.5), black carbon (BC), and nitrogen dioxide (NO2) were determined based on land use regression models of street-level pollution measured by the New York City Community Air Survey. Spatial data were categorized using k-means cluster analysis and clusters were associated with air pollution using analysis of variance.Results: Based on significant correlations with air pollutants, three geographic indicators were included for cluster analysis: number of bus stops; truck route density (total km route/km2 land); and percentage of area covered with trees (i.e. tree canopy). Four clusters were identified: 1. Higher truck route density (n=103 schools); 2. Higher number of bus stops (n=378); 3. Higher tree canopy (n=250); and 4. Lower in all 3 indicators (n=453). In general, the levels of PM2.5, BC, and NO2 were highest among schools with higher truck route density, followed by higher number of bus stops, and lowest with higher tree canopy (p=0.001).Conclusions: School-aged children may experience higher levels of air pollution based on their school’s proximity to geographic indicators of diesel vehicle emission. Geographic indicators may serve as surrogates of chronic school exposure to air pollution. Future studies will determine if clusters are associated with school asthma prevalence.

Association between exposure to traffic-related air pollution and pediatric allergic diseases based on modeled air pollution concentrations and traffic measures in Seoul, Korea: a comparative analysis

BackgroundPediatric allergic diseases are a major public health concern, and previous studies have suggested that exposure to traffic-related air pollution (TRAP) exposure is a risk factor. These studies have typically assessed TRAP exposure using traffic measures, such as distance to major roads, or by modeling air pollutant concentrations; however inconsistent associations with pediatric allergic diseases have often been found. Using road proximity and density, we previously found an association between TRAP and atopic eczema among approximately 15,000 children living in Seoul, Korea, heavily populated and highly polluted city in which traffic is a major emission source. We aimed to conduct a parallel analysis using modeled air pollution concentrations and thus examine the consistency of the association. Specifically, we examined the associations of individual-level annual-average concentrations of NO2, PM10, and PM2.5 with symptoms and diagnoses of three pediatric allergic diseases including asthma, allergic rhinitis, and atopic eczema.MethodsThe study population included 14,614 children from the Seoul Atopy Friendly School Project Survey in Seoul, Korea, in 2010. To assess individual exposures to TRAP among these children, we predicted annual-average concentrations of NO2, PM10, and PM2.5 at the children’s home addresses in 2010 using universal kriging and land use regression models along with regulatory air quality monitoring data and geographic characteristics. Then, we estimated odds ratios (ORs) of the three allergic diseases for interquartile increases in air pollution concentrations after adjusting for individual risk factors in mixed effects logistic regression.ResultsSymptoms and diagnoses of atopic eczema symptoms showed an association with NO2 (OR = 1.07, 95% confidence interval = 1.02–1.13; 1.08, 1.03–1.14) and PM10 (1.06, 1.01–1.12; 1.07, 1.01–1.13). ORs of PM2.5 were positive but not statistically significant (1.01, 0.95–1.07; 1.04, 0.98–1.10). No association was found between asthma and allergic rhinitis, although PM2.5 showed a marginal association with allergic rhinitis.ConclusionsOur consistent findings regarding the association between TRAP and the prevalence of atopic eczema using traffic measures and surrogate air pollutants suggested the effect of TRAP on children’s health. Follow-up studies should elucidate the causal link, to support subsequent policy considerations and minimize adverse health effects in children.

Myo-inositol mediates the effects of traffic-related air pollution on generalized anxiety symptoms at age 12 years

BackgroundExposure to traffic-related air pollution (TRAP) has been linked to childhood anxiety symptoms. Neuroimaging in patients with anxiety disorders indicate altered neurochemistry. ObjectivesEvaluate the impact of TRAP on brain metabolism and its relation to childhood anxiety symptoms in the Cincinnati Childhood Allergy and Air Pollution Study (CCAAPS). MethodsAdolescents (n = 145) underwent magnetic resonance spectroscopy. Brain metabolites, including myo-inositol, N-acetylaspartate, creatine, choline, glutamate, glutamate plus glutamine, and glutathione were measured in the anterior cingulate cortex. Anxiety symptoms were assessed using the Spence Children's Anxiety Scale. TRAP exposure in early-life, averaged over childhood, and during the 12 months prior to imaging was estimated using a validated land use regression model. Associations between TRAP exposure, brain metabolism, and anxiety symptoms were estimated using linear regression and a bootstrapping approach for testing mediation by brain metabolite levels. ResultsRecent exposure to high levels of TRAP was associated with significant increases in myo-inositol (β = 0.26; 95%CI 0.01, 0.51) compared to low TRAP exposure. Recent elevated TRAP exposure (β = 4.71; 95% CI 0.95, 8.45) and increased myo-inositol levels (β = 2.98; 95% CI 0.43, 5.52) were also significantly associated with increased generalized anxiety symptoms with 12% of the total effect between TRAP and generalized anxiety symptoms being mediated by myo-inositol levels. ConclusionsThis is the first study of children to utilize neuroimaging to link TRAP exposure, metabolite dysregulation in the brain, and generalized anxiety symptoms among otherwise healthy children. TRAP may elicit atypical excitatory neurotransmission and glial inflammatory responses leading to increased metabolite levels and subsequent anxiety symptoms.

Prenatal and early life exposure to air pollution induced hippocampal vascular leakage and impaired neurogenesis in association with behavioral deficits

Exposure to traffic-related air pollution (TRAP) is associated with a range of neurodevelopmental disorders in human populations. In rodent models, prenatal TRAP exposure increased depressive behaviors and increased brain microglial activity. To identify cellular mechanisms, we examined adult neurogenesis and the blood–brain barrier (BBB) in relation to cognition and motivated behaviors in rats that were exposed to a nano-sized TRAP subfraction from gestation into adulthood. At age 5 months, exposed male rats had 70% fewer newly generated neurons in the dentate gyrus (DG) of the hippocampus. Microglia were activated in DG and CA1 subfields (35% more Iba1). The BBB was altered, with a 75% decrease of the tight junction protein ZO-1 in the CA1 layer, and twofold more iron deposits, a marker of microhemorrhages. The exposed rats had impaired contextual memory (novel object in context), reduced food-seeking behavior, and increased depressive behaviors (forced swim). Deficits of de novo neurogenesis were inversely correlated with depressive behavior, whereas increased microbleeds were inversely correlated with deficits in contextual memory. These findings give the first evidence that prenatal and early life exposure to TRAP impairs adult hippocampal neurogenesis and increases microbleeds in association with behavioral deficits.

Chronic exposure to traffic-related air pollution and cancer incidence among 10,000 patients undergoing percutaneous coronary interventions: A historical prospective study.

Background Exposure to traffic-related air pollution (TRAP) is considered to have a carcinogenic effect. The authors previously reported a nonsignificant association between TRAP and cancer risk in a relatively small cohort of myocardial infarction survivors. This study assessed whether TRAP exposure is associated with subsequent cancer in a large cohort of coronary patients. Methods & results Consecutive patients undergoing percutaneous coronary interventions in a major medical centre in central Israel from 2004 to 2014 were followed for cancer through 2015. Residential levels of nitrogen oxides (NOx) - a proxy for TRAP - were estimated based on a high-resolution national land use regression model. Cox proportional hazards models were constructed to study relationships with cancer. Among 12,784 candidate patients, 9816 had available exposure data and no history of cancer (mean age, 68 years; 77% men). During a median (25th-75th percentiles) follow-up of 7.0 (3.9-9.3) years, 773 incident cases of cancer (8%) were diagnosed. In a multivariable-adjusted model, a 10-ppb increase in mean NOx exposure was associated with hazard ratios (HRs) of 1.07 (95% confidence interval [CI] 1.00-1.15) for all-site cancer and 1.16 (95% CI 1.05-1.28) for cancers previously linked to TRAP (lung, breast, prostate, kidney and bladder). A stronger association was observed for breast cancer (HR = 1.43; 95% CI 1.12-1.83). Associations were slightly strengthened after limiting the cohort to patients with more precise exposure assessment. Conclusion Coronary patients exposed to TRAP are at increased risk of several types of cancer, particularly lung, prostate and breast. As these cancers are amenable to prevention strategies, identifying highly exposed patients may provide an opportunity to improve clinical care.