Traffic-related Air Pollution Exposure Research Articles

Traffic Related Air Pollution Exposure Effect on Circulating White Blood Cell Counts in Healthy Individuals

During this short term study a total of 110 samples were collected from the selected individuals of study area. This study was aimed to count the White blood cells in the blood samples of individuals, who were mostly exposed to exhaust fumes (air pollution), like traffic constables, cooks and shopkeepers. For this purpose blood samples were taken into an evacuee container having anticoagulant Ethylene diamine tetra-acetic acid (EDTA) so to prevent coagulation of blood, for the count of WBCs, heamocyto-meter was used. During the study the body mass index and blood pressure was also measured by digital blood pressure measuring apparatus. Samples were observed under the microscope. It was found that 15% (13,133±2544.081) sampled individuals had increased WBCs and 85% (7821±1482.76) normal WBCs. In female samples 50% (11900±2151.27) were observed with above range of WBCs and other 50% (8540±844.39) with normal range of WBCs count, non-had WBCs count lower than the normal WBCs. Mostly had normal and few had above the range. One way ANOVA has been used to analyze connection of exposure to air pollution with counts of circulating white blood cells.

Traffic-related air pollution is associated with glucose dysregulation, blood pressure, and oxidative stress in children

BackgroundMetabolic syndrome increases the risk of cardiovascular disease in adults. Antecedents likely begin in childhood and whether childhood exposure to air pollution plays a contributory role is not well understood. ObjectivesTo assess whether children's exposure to air pollution is associated with markers of risk for metabolic syndrome and oxidative stress, a hypothesized mediator of air pollution-related health effects. MethodsWe studied 299 children (ages 6–8) living in the Fresno, CA area. At a study center visit, questionnaire and biomarker data were collected. Outcomes included hemoglobin A1c (HbA1c), urinary 8-isoprostane, systolic blood pressure (SBP), and BMI. Individual-level exposure estimates for a set of four pollutants that are constituents of traffic-related air pollution (TRAP) – the sum of 4-, 5-, and 6-ring polycyclic aromatic hydrocarbon compounds (PAH456), NO2, elemental carbon, and fine particulate matter (PM2.5) – were modeled at the primary residential location for 1-day lag, and 1-week, 1-month, 3-month, 6-month, and 1-year averages prior to each participant's visit date. Generalized additive models were used to estimate associations between each air pollutant exposure and outcome. ResultsThe study population was 53% male, 80% Latinx, 11% Black and largely low-income (6% were White and 3% were Asian/Pacific Islander). HbA1c percentage was associated with longer-term increases in TRAP; for example a 4.42 ng/m3 increase in 6-month average PAH456 was associated with a 0.07% increase (95% CI: 0.01, 0.14) and a 3.62 μg/m3 increase in 6-month average PM2.5 was associated with a 0.06% increase (95% CI: 0.01, 0.10). The influence of air pollutants on blood pressure was strongest at 3 months; for example, a 6.2 ppb increase in 3-month average NO2 was associated with a 9.4 mmHg increase in SBP (95% CI: 2.8, 15.9). TRAP concentrations were not significantly associated with anthropometric or adipokine measures. Short-term TRAP exposure averages were significantly associated with creatinine-adjusted urinary 8-isoprostane. DiscussionOur results suggest that both short- and longer-term estimated individual-level outdoor residential exposures to several traffic-related air pollutants, including ambient PAHs, are associated with biomarkers of risk for metabolic syndrome and oxidative stress in children.

Metabolomics analysis of maternal serum exposed to high air pollution during pregnancy and risk of autism spectrum disorder in offspring

BackgroundPreviously, numerous epidemiologic studies reported an association between autism spectrum disorder (ASD) and exposure to air pollution during pregnancy. However, there have been no metabolomics studies investigating the impact of pregnancy pollution exposure to ASD risk in offspring. ObjectivesTo identify differences in maternal metabolism that may reflect a biological response to exposure to high air pollution in pregnancies of offspring who later did or did not develop ASD. MethodsWe obtained stored mid-pregnancy serum from 214 mothers who lived in California's Central Valley and experienced the highest levels of air pollution during early pregnancy. We estimated each woman's average traffic-related air pollution exposure (carbon monoxide, nitric oxides, and particulate matter <2.5 μm) during the first trimester using the California Line Source Dispersion Model, version 4 (CALINE4). By utilizing liquid chromatography-high resolution mass spectrometry, we identified the metabolic profiles of maternal serum for 116 mothers with offspring who later developed ASD and 98 control mothers. Partial least squares discriminant analysis (PLS-DA) was employed to select metabolic features associated with air pollution exposure or autism risk in offspring. We also conducted extensive pathway enrichment analysis to elucidate potential ASD-related changes in the metabolome of pregnant women. ResultsWe extracted 4022 and 4945 metabolic features from maternal serum samples in hydrophilic interaction (HILIC) chromatography (positive ion mode) and C18 (negative ion mode) columns, respectively. After controlling for potential confounders, we identified 167 and 222 discriminative features (HILIC and C18, respectively). Pathway enrichment analysis to discriminate metabolic features associated with ASD risk indicated various metabolic pathway perturbations linked to the tricarboxylic acid (TCA) cycle and mitochondrial function, including carnitine shuttle, amino acid metabolism, bile acid metabolism, and vitamin A metabolism. ConclusionUsing high resolution metabolomics, we identified several metabolic pathways disturbed in mothers with ASD offspring among women experiencing high exposure to traffic-related air pollution during pregnancy that were associated with mitochondrial dysfunction. These findings provide us with a better understanding of metabolic disturbances involved in the development of ASD under adverse environmental conditions.

Trace element concentrations in ambient air as a function of distance from road

ABSTRACT Traffic-related air pollution is associated with various adverse health effects. In the absence of more complicated exposure assessment techniques, many environmental health studies have used the natural logarithm of distance to road as a proxy for traffic-related exposures. However, research validating this proxy and further explaining the spatial patterns and elemental composition of traffic-related particulate matter air pollution remains limited. In this study, we collected air samples using a mobile particle concentrator that allowed for high sample loading from major roadways in the Greater Boston Area. We found that concentrations of Cl, Ti, V, Cr, Mn, Fe, Co, Cu, Zn, Sr, Zr, Sn, Ba, and Pb were significantly associated with the natural logarithm of distance to road in coarse particulate matter, and total fine particulate mass concentrations of Al, Ca, Ti, Cr, Mn, Fe, Cu, and Zn were significantly associated with natural logarithm of distance to road in fine particulate matter. Road type (A1 or A2 [primary roads or highways] versus A3 [secondary and connecting roads]) was not a significant predictor of any traffic-related elements in particulate matter air pollution. Our results help identify traffic-related elements in particulate matter air pollution and support the use of logarithm of distance to road as a proxy for traffic-related particulate matter air pollution exposure assessment in epidemiological studies.

Proximity to traffic and exposure to polycyclic aromatic hydrocarbons in relation to Attention Deficit Hyperactivity Disorder and conduct disorder in U.S. children.

Traffic related air pollution (TRAP) and its component polycyclic aromatic hydrocarbons (PAHs) may be neurotoxic in children. There is limited research on postnatal exposure to TRAP and PAHs and child neurodevelopment. We linked data from the U.S. NHANES 2001-2004 with the National Highway Planning Network 2005 to examine the proximity to major roads (highway or urban/rural principal arterials), urinary PAH metabolites, and diagnosis of Attention Deficit Hyperactivity Disorder (ADHD) and Conduct Disorder (CD) based on Diagnostic Interview Schedule for Children (C-DISC) in 1253 children aged 8-15 years. We calculated odds ratios (ORs) and 95% Confidence Intervals (CIs) for ADHD and CD by traffic proximity and PAH exposures using logistic regression adjusted for confounders. Higher ADHD prevalence was observed among children living <500m (9.86%) compared to those ≥500m (3.84%) from a major road. Prevalence of children with CD was comparable (<500m: 2.51% and ≥500m: 2.43%). We found little difference in urinary PAH metabolite levels between children living near major roads and those who did not. Children living <500m from a major road had a non-significant OR of 2.06 (95% CI 0.85-5.03) for ADHD diagnosis. Children living on ≥2 major roads within 500m of a highway had a non-significant OR of 2.27 (95% CI 0.71-7.26) for ADHD diagnosis. There was no association between proximity to major roads and CD diagnosis. We found living close to a major road was not associated with increased PAH levels. We did not find statistically significant relation between proximity to a major road or urinary PAH metabolite levels and ADHD or CD diagnosis in this cross-sectional analysis. Prospective studies are needed for the investigation of postnatal TRAP exposure and ADHD and CD diagnosis.

Four Decades of United States Mobile Source Pollutants: Spatial-Temporal Trends Assessed by Ground-Based Monitors, Air Quality Models, and Satellites.

On-road emissions sources degrade air quality, and these sources have been highly regulated. Epidemiological and environmental justice studies often use road proximity as a proxy for traffic-related air pollution (TRAP) exposure, and other studies employ air quality models or satellite observations. To assess these metrics' abilities to reproduce observed near-road concentration gradients and changes over time, we apply a hierarchical linear regression to ground-based observations, long-term air quality model simulations using Community Multiscale Air Quality (CMAQ), and satellite products. Across 1980-2019, observed TRAP concentrations decreased, and road proximity was positively correlated with TRAP. For all pollutants, concentrations decreased fastest at locations with higher road proximity, resulting in "flatter" concentration fields in recent years. This flattening unfolded at a relatively constant rate for NOx, whereas the flattening of CO concentration fields has slowed. CMAQ largely captures observed spatial-temporal NO2 trends across 2002-2010 but overstates the relationships between CO and elemental carbon fine particulate matter (EC) road proximity. Satellite NOx measures overstate concentration reductions near roads. We show how this perspective provides evidence that California's on-road vehicle regulations led to substantial decreases in NO2, NOx, and EC in California, with other states that adopted California's light-duty automobile standards showing mixed benefits over states that did not adopt these standards.

Respiratory Effects of Exposure to Traffic-Related Air Pollutants During Exercise.

Traffic-related air pollution (TRAP) is increasing worldwide. Habitual physical activity is known to prevent cardiorespiratory diseases and mortality, but whether exposure to TRAP during exercise affects respiratory health is still uncertain. Exercise causes inflammatory changes in the airways, and its interaction with the effects of TRAP or ozone might be detrimental, for both athletes exercising outdoor and urban active commuters. In this Mini-Review, we summarize the literature on the effects of exposure to TRAP and/or ozone during exercise on lung function, respiratory symptoms, performance, and biomarkers. Ozone negatively affected pulmonary function after exercise, especially after combined exposure to ozone and diesel exhaust (DE). Spirometric changes after exercise during exposure to particulate matter and ultrafine particles suggest a decrease in lung function, especially in patients with chronic obstructive pulmonary disease. Ozone frequently caused respiratory symptoms during exercise. Women showed decreased exercise performance and higher symptom prevalence than men during TRAP exposure. However, performance was analyzed in few studies. To date, research has not identified reliable biomarkers of TRAP-related lung damage useful for monitoring athletes' health, except in scarce studies on airway cells obtained by induced sputum or bronchoalveolar lavage. In conclusion, despite partly counteracted by the positive effects of habitual exercise, the negative effects of TRAP exposure to pollutants during exercise are hard to assess: outdoor exercise is a complex model, for multiple and variable exposures to air pollutants and pollutant concentrations. Further studies are needed to identify pollutant and/or time thresholds for performing safe outdoor exercise in cities.

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.

Metabolic dysfunction modifies the influence of traffic-related air pollution and noise exposure on late-life dementia and cognitive impairment: A cohort study of older Mexican-Americans.

For 1,612 elderly Mexican-American participants of the Sacramento Area Latino Study on Aging (SALSA) followed for up to 10 years, we estimated residential-based local traffic-related exposures relying on the California Line Source Dispersion Model version 4 (CALINE4) for nitrogen oxides (NOx) and the SoundPLAN software package (Version 8.0; NAVCON, Fullerton, CA) that implements the Federal Highway Administration Traffic Noise Model (TNM) for noise, respectively. We used Cox proportional hazard models to estimate the joint effects of NOx or noise exposures and obesity, hyperglycemia, or low high-density lipoprotein (HDL) cholesterol. The risk of developing dementia/CIND among participants with hyperglycemia who also were exposed to high levels of NOx (≥3.44 parts per billion [ppb] [75th percentile]) or noise (≥65 dB) was 2.4 (1.4, 4.0) and 2.2 (1.7, 3.9), respectively. For participants with low HDL-cholesterol, the estimated hazard ratios for dementia/CIND were 2.5 (1.4, 4.3) and 1.8 (1.0, 3.0) for those also exposed to high levels of NOx (≥3.44 ppb) or noise (≥65 dB), respectively, compared with those without metabolic dysfunction exposed to low traffic-related air pollution or noise levels. Exposure to traffic-related air pollution or noise most strongly increases the risk of dementia/CIND among older Mexican-Americans living in California who also exhibit hyperglycemia or low HDL-cholesterol.

Pathological Cardiopulmonary Evaluation of Rats Chronically Exposed to Traffic-Related Air Pollution.

Background:Traffic-related air pollution (TRAP) is made up of complex mixtures of particulate matter, gases and volatile compounds. However, the effects of TRAP on the cardiopulmonary system in most animal studies have been tested using acute exposure to singular pollutants. The cardiopulmonary effects and molecular mechanisms in animals that are chronically exposed to unmodified air pollution as a whole have yet to be studied. Additionally, sex-dependent toxicity of TRAP exposure has rarely been evaluated.Objectives:This study sought to assess the cardiopulmonary effect of chronic exposure to unmodified, real-world TRAP in both female and male rats.Methods:Four-week-old male and female rats were exposed to TRAP or filtered air for 14 months in a novel facility drawing air from a major freeway tunnel system in Northern California. Inflammation and oxidative stress markers were examined in the lung, heart, spleen, and plasma, and TRAP deposits were quantified in the lungs of both male and female rats.Results:Elemental analysis showed higher levels of eight elements in the female lungs and one element in the male lungs. Expression of genes related to fibrosis, aging, oxidative stress, and inflammation were higher in the rat hearts exposed to TRAP, with female rats being more susceptible than males. Enhanced collagen accumulation was found only in the TRAP-exposed female hearts. Plasma cytokine secretion was higher in both female and male rats, but inflammatory macrophages were higher only in TRAP-exposed male spleens.Discussion:Our results in rats suggest pathological consequences from chronic TRAP exposure, including sex differences indicating females may be more susceptible to TRAP-induced cardiac fibrosis. https://doi.org/10.1289/EHP7045

Residential proximity to major roads and fecundability in a preconception cohort.

Among 7,342 female pregnancy planners from the United States and 1,448 from Canada, we examined the association between residential proximity to major roads and fecundability, the per-cycle probability of conception. From 2013 to 2019, women 21-45 years old who were trying to conceive without fertility treatment completed an online baseline questionnaire and follow-up questionnaires every 8 weeks for up to 12 months or until pregnancy. We geocoded residential addresses reported at baseline and during follow-up, and calculated distance to nearest major roads and length of major roads within buffers of 50, 100, 300, and 400 meters around the residence as proxies for traffic-related air pollution. We used proportional probabilities regression models to estimate fecundability ratios (FRs) and 95% confidence intervals (CIs), adjusting for individual- and neighborhood-level characteristics. In the United States, the FR comparing women who lived <50 meters with those who lived ≥400 meters from the closest major road was 0.88 (95% CI = 0.80, 0.98). The association among Canadian women was similar in magnitude, but less precise (FR = 0.93; 95% CI = 0.74, 1.16). Likewise, length of major roads within buffers of 50 and 100 meters was associated with lower fecundability in both countries; associations were attenuated within larger buffers. These results are consistent with the hypothesis that traffic-related air pollution or other near-road exposures may adversely affect fecundability.

Application of high-resolution metabolomics to identify biological pathways perturbed by traffic-related air pollution

BackgroundSubstantial research has investigated the adverse effects of traffic-related air pollutants (TRAP) on human health. Convincing associations between TRAP and respiratory and cardiovascular diseases are known, but the underlying biological mechanisms are not well established. High-resolution metabolomics (HRM) is a promising platform for untargeted characterization of molecular mechanisms between TRAP and health indexes. ObjectivesWe examined metabolic perturbations associated with short-term exposures to TRAP, including carbon monoxide (CO), nitrogen dioxide (NO2), ozone (O3), fine particulate matter (PM2.5), organic carbon (OC), and elemental carbon (EC) among 180 participants of the Center for Health Discovery and Well-Being (CHDWB), a cohort of Emory University-affiliated employees. MethodsA cross-sectional study was conducted on baseline visits of 180 CHDWB participants enrolled during 2008–2012, in whom HRM profiling was determined in plasma samples using liquid chromatography-high-resolution mass spectrometry with positive and negative electrospray ionization (ESI) modes. Ambient pollution concentrations were measured at an ambient monitor near downtown Atlanta. Metabolic perturbations associated with TRAP exposures were assessed following an untargeted metabolome-wide association study (MWAS) framework using feature-specific Tobit regression models, followed by enriched pathway analysis and chemical annotation. ResultsSubjects were predominantly white (76.1%) and non-smokers (95.6%), and all had at least a high school education. In total, 7821 and 4123 metabolic features were extracted from the plasma samples by the negative and positive ESI runs, respectively. There are 3421 features significantly associated with at least one air pollutant by negative ion mode, and 1691 features by positive ion mode. Biological pathways enriched by features associated with the pollutants are primarily involved in nucleic acids damage/repair (e.g., pyrimidine metabolism), nutrient metabolism (e.g., fatty acid metabolism), and acute inflammation (e.g., histidine metabolism and tyrosine metabolism). NO2 and EC were associated most consistently with these pathways. We confirmed the chemical identity of 8 metabolic features in negative ESI and 2 features in positive ESI, including metabolites closely linked to oxidative stress and inflammation, such as histamine, tyrosine, tryptophan, and proline. ConclusionsWe identified a range of ambient pollutants, including components of TRAP, associated with differences in the metabolic phenotype among the cohort of 180 subjects. We found Tobit models to be a robust approach to handle missing data among the metabolic features. The results were encouraging of further use of HRM and MWAS approaches for characterizing molecular mechanisms underlying exposure to TRAP.

Two communities, one highway and the fight for clean air: the role of political history in shaping community engagement and environmental health research translation

BackgroundThis paper explores strategies to engage community stakeholders in efforts to address the effects of traffic-related air pollution (TRAP). Communities of color and low-income communities are disproportionately impacted by environmental threats including emissions generated by major roadways.MethodsQualitative instrumental case study design was employed to examine how community-level factors in two Massachusetts communities, the City of Somerville and Boston’s Chinatown neighborhood, influence the translation of research into practice to address TRAP exposure. Guided by the Interactive Systems Framework (ISF), we drew on three data sources: key informant interviews, observations and document reviews. Thematic analysis was used.ResultsFindings indicate political history plays a significant role in shaping community action. In Somerville, community organizers worked with city and state officials, and embraced community development strategies to engage residents. In contrast, Chinatown community activists focused on immediate resident concerns including housing and resident displacement resulting in more opposition to local municipal leadership.ConclusionsThe ISF was helpful in informing the team’s thinking related to systems and structures needed to translate research to practice. However, although municipal stakeholders are increasingly sympathetic to and aware of the health impacts of TRAP, there was not a local legislative or regulatory precedent on how to move some of the proposed TRAP-related policies into practice. As such, we found that pairing the ISF with a community organizing framework may serve as a useful approach for examining the dynamic relationship between science, community engagement and environmental research translation. Social workers and public health professionals can advance TRAP exposure mitigation by exploring the political and social context of communities and working to bridge research and community action.

Association BetweenPM2.5Exposure and Preeclampsia

Background: Previous studies have suggested that traffic-related air pollution can increase risk of pregnancy complications. The purpose of this research is to investigate if PM2.5 exposure one year prior to conception is associated with preeclampsia. Methods: We obtained all live and still births from the Massachusetts state birth registry with an estimated conception date between January 2002 through December 2008. We randomly selected 2,000 infants conceived each year to serve as the study population. Of those 14,000 births, all mothers diagnosed with the main symptoms of preeclampsia, high blood pressure or proteinuria, were identified as cases. Cumulative PM2.5 exposure was assessed using 4-km spatial satellite remote sensing, meteorological and land use spatiotemporal models at geocoded birth addresses for the year prior to conception. We calculated crude and adjusted preeclampsia odds ratios (ORs) and 95% confidence intervals (CI) per 10 µg/m3 increase of PM2.5 exposure. Analyses of complete data were adjusted for demographic, socioeconomic, and reproductive characteristics of the mother. Births missing over 70% of PM2.5 data were excluded. Results: Our final analyses included 576 cases and 11,679 controls. Cumulative PM2.5 exposure during the year prior to conception was not associated with preeclampsia in the unadjusted analyses (OR: 1.02; 95%CI: 0.97,1.07). After adjusting for maternal age, race, education, language, insurance status, parity, smoking, drinking, adequacy of care, and year of birth, PM2.5 exposure remained not significantly associated with preeclampsia (OR: 1.04; 95%CI: 0.98,1.10). As confirmed by prior literature, Non-Hispanic Black mothers had almost double the risk of being a case compared to the referent group (Non-Hispanic White) (OR: 1.89; 95%CI: 1.44,2.48). Discussion: We did not find evidence to support the relationship between maternal traffic related air pollution exposure and preeclampsia. Future work will assess whether other areas with a higher threshold of air pollution exposure would be associated with preeclampsia.

Street Vendors in Kampala, Uganda: Traffic-related Air Pollution Exposure and Adverse Health Experiences.

BACKGROUND: Health effects due to street vending have limited epidemiological research. Street vending is a dominant occupation in developing cities and individuals engaged in this venture are exposed to high levels of traffic related air pollution (TRAP) per mode of operation. OBJECTIVE: To establish the TRAP exposure experiences of street vendors in Kampala and associated adverse respiratory, cardiovascular, reproductive and musculoskeletal health effects. METHODS: A cross-sectional study was conducted among 418 street vendors operating in commercial areas of Kampala. Exposure to TRAP was categorized as low, moderate and high on the basis of street vending activity levels and self-reported traffic density in vending areas. Low-cost air sensors were used to monitor air quality in the vending areas over a three-day period with levels of PM2.5 found to exceed the WHO recommended levels. RESULTS: Street vendors that reported high traffic density in vending areas had 2.68(95%CI: 1.47, 4.88), 2.91(95%CI: 1.18, 7.14) and 1.79(95%CI: 1.03, 3.11) increased odds of cough and catarrh, compared to their counterparts who reported low traffic density in vending areas. Moderate vending activity levels were associated with 2.25(95%CI: 1.00, 5.05) increased odds of sharp chest pains compared to low vending activity levels. Street vendors who reported moderate and high traffic density in vending areas had 3.00(95%CI: 1.23, 7.36) and 4.24(95%CI: 1.73, 10.38) increased odds of difficulty in walking. Moderate TRAP exposure was associated with 1.76(95%CI: 1.11, 2.79), 1.02(95%CI: 1.02, 2.70) and 2.17(95%CI: 1.09, 4.31) increased odds of catarrh, sneezing and difficulty in kneeling respectively. CONCLUSION: street vending and air pollution exposure was found to be associated with various adverse health outcomes in this population. Genome-wide association studies exploring the biological mechanisms of respiratory and cardiovascular injury from exposure to air pollution among street vendors is recommended to help better tailor treatment and preventive strategies.

The Relationship between Traffic-Related Air Pollution Exposures and Allostatic Load among Youth with Type 1 Diabetes in the SEARCH Cohort

Background/Aim: We investigated the effects of chronic exposures to particulate and traffic-related air pollution on allostatic load (AL), a marker of cumulative biological risk, among youth with type 1 diabetes. Methods: Participants were drawn from five clinical sites of the SEARCH for Diabetes in Youth study (n=2,338). Baseline questionnaires, anthropometric measures, and a fasting blood test were taken at a clinic visit between 2001 and 2005. AL was calculated using 10 biomarkers reflecting cardiovascular, metabolic, and inflammatory risk. Monthly and annual residential exposures to particulate matter &lt; 2.5 µm in diameter (PM2.5) and proximity to heavily-trafficked major roadways were estimated for each participant. Separate linear mixed models adjusted for sociodemographic and lifestyle factors were conducted for each exposure. Results: No significant associations were observed between exposures to PM2.5 or proximity to traffic and AL in our main analysis. However, several associations were identified in stratified analyses. Among non-white participants, an interquartile range (IQR) increase in monthly average PM2.5 was inversely associated with AL (β=-0.18, 95% CI: -0.36, -0.01), while residing in proximity to heavily-trafficked major roadways was positively associated with AL (β=0.73, 95% CI: 0.19, 1.3) and the cardiovascular and inflammatory AL subscales. Among non-Hispanic white participants and female participants, an IQR increase in monthly average PM2.5 was positively associated with the inflammatory AL subscale (β=0.10, 95% CI: 0.03, 0.18 and β=0.11, 95% CI: 0.02, 0.20, respectively). Conclusions: Among youth with type 1 diabetes, the effects of chronic exposures to particulate and traffic-related air pollution on AL and its subscales may differ by race/ethnicity and sex.

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.

Traffic-related NOx exposure and proximity to freeways are related to adverse changes in subclinical atherosclerosis measures from childhood to adulthood

Background: Chronic exposure to air pollutants is associated with increased risk of cardiovascular disease (CVD) among adults. However, little is known about how air pollution may affect the development of subclinical atherosclerosis in younger populations. Subclinical measures of atherosclerosis, including carotid artery intima-media thickness (CIMT) and arterial stiffness (CAS), may provide insight into early CVD pathogenesis. Methods: In a pilot study of 70 participants from the Southern California Children’s Health Study, we investigated subclinical atherosclerosis progression from childhood to adulthood. Using carotid artery ultrasound images obtained at age 10 and follow-up images from age 21-22, we examined associations between traffic-related pollutants and changes in CIMT and CAS. Lifetime average traffic-related NOx exposures were assigned using the CALINE4 (California Line Source) dispersion model. Distance to nearest roadways by class was assigned based on ESRI Streetmap Premium roadway data. Results: For each interquartile range increase in average lifetime NOx exposure, we observed a 12.12μm (95% CI: 1.11-23.13; p=0.03) increase in early adulthood attained CIMT and greater longitudinal changes in CIMT from childhood to adulthood (11.5μm, 95% CI: 1.29-21.73, p=0.03) over the follow-up period. Similar adverse changes in CIMT were observed with distance to nearest freeway. Changes in CAS were related to distance to freeway, such that living in closer proximity to freeways was related to greater adverse change in CAS over the follow-up period (stiffness index beta: 0.85; 95% CI: 1.50, 0.21, p=0.01; distensibility: -5.61; 95% CI: -0.93, -10.27, p=0.02).Conclusions: We observed greater adverse changes measures of carotid artery wall thickness and stiffness over time in relation to lifetime traffic-related NOx exposure and residential proximity to freeways. To our knowledge, this is the first study to evaluate the longitudinal impact of lifetime traffic-related air pollution exposure on changes in subclinical markers of atherosclerosis during the critical transition from childhood to adulthood.

Short-term health effects of traffic-related air pollution exposures in multi-modal commuting in Chengdu, China

Short-term health effects of traffic-related air pollution exposures in multi-modal commuting in Chengdu, China

Effects of low exposure to traffic related air pollution on childhood asthma onset by age 10 years

Although NO2, a major traffic related air pollutant, has been associated with onset of childhood asthma, young children may be more susceptible to traffic related air pollution exposure compared to other individuals. We linked data from National Longitudinal Survey of Children and Youths Cycle 1–5 (1994–2003) and the National Air Pollution Surveillance Program to determine the association between NO2 exposure and either early or late onset childhood asthma phenotypes. Children diagnosed with asthma from age 0–3 were defined as having early onset asthma. Children diagnosed with asthma from age 4–9 were defined as having late onset asthma. Mean NO2 exposure for each quartile was 6.31 ppb, 9.45 ppb, 11.83 ppb, and 17.9 ppb. Higher levels of NO2 exposure were more strongly associated with early childhood asthma (Quartile 3 OR: 2.11, 95% CI: 1.29, 3.44, Quartile 4 OR: 2.16, 95% CI: 1.27, 3.68) compared to the lowest level of NO2 exposure (Quartile 1). No such association was observed with risk of late childhood asthma onset. Asthma susceptibility to NO2 exposure may vary with the childhood developmental stage, and young children may be susceptible to NO2 exposure at levels well below national and international guidelines. Our study emphasizes the importance of considering the timing of childhood asthma onset in future studies and confirms the increased risk of early onset of childhood asthma associated even with relatively low NO2 exposure levels.