Traffic-related Air Pollution Research Articles

Multiomic Signatures of Traffic-Related Air Pollution in London Reveal Potential Short-Term Perturbations in Gut Microbiome-Related Pathways.

This randomized crossover study investigated the metabolic and mRNA alterations associated with exposure to high and low traffic-related air pollution (TRAP) in 50 participants who were either healthy or were diagnosed with chronic pulmonary obstructive disease (COPD) or ischemic heart disease (IHD). For the first time, this study combined transcriptomics and serum metabolomics measured in the same participants over multiple time points (2 h before, and 2 and 24 h after exposure) and over two contrasted exposure regimes to identify potential multiomic modifications linked to TRAP exposure. With a multivariate normal model, we identified 78 metabolic features and 53 mRNA features associated with at least one TRAP exposure. Nitrogen dioxide (NO2) emerged as the dominant pollutant, with 67 unique associated metabolomic features. Pathway analysis and annotation of metabolic features consistently indicated perturbations in the tryptophan metabolism associated with NO2 exposure, particularly in the gut-microbiome-associated indole pathway. Conditional multiomics networks revealed complex and intricate mechanisms associated with TRAP exposure, with some effects persisting 24 h after exposure. Our findings indicate that exposure to TRAP can alter important physiological mechanisms even after a short-term exposure of a 2 h walk. We describe for the first time a potential link between NO2 exposure and perturbation of the microbiome-related pathways.

Societal Co-benefits of Zero-Emission Vehicles in the Freight Industry.

This study was set in the Greater Toronto and Hamilton Area (GTHA), where commercial vehicle movements were assigned across the road network. Implications for greenhouse gas (GHG) emissions, air quality, and health were examined through an environmental justice lens. Electrification of light-, medium-, and heavy-duty trucks was assessed to identify scenarios associated with the highest benefits for the most disadvantaged communities. Using spatially and temporally resolved commercial vehicle movements and a chemical transport model, changes in air pollutant concentrations under electric truck scenarios were estimated at 1-km2 resolution. Heavy-duty truck electrification reduces ambient black carbon and nitrogen dioxide on average by 10 and 14%, respectively, and GHG emissions by 10.5%. It achieves the highest reduction in premature mortality attributable to fine particulate matter chronic exposure (around 200 cases per year) compared with light- and medium-duty electrification (less than 150 cases each). The burden of all traffic in the GTHA was estimated to be around 600 cases per year. The benefits of electrification accrue primarily in neighborhoods with a high social disadvantage, measured by the Ontario Marginalization Indices, narrowing the disparity of exposure to traffic-related air pollution. Benefits related to heavy-duty truck electrification reflect the adverse impacts of diesel-fueled freight and highlight the co-benefits achieved by electrifying this sector.

A nested case-control study of untargeted plasma metabolomics and lung cancer among never-smoking women within the prospective Shanghai Women's Health Study.

The etiology of lung cancer in never-smokers remains elusive, despite 15% of lung cancer cases in men and 53% in women worldwide being unrelated to smoking. Here, we aimed to enhance our understanding of lung cancer pathogenesis among never-smokers using untargeted metabolomics. This nested case-control study included 395 never-smoking women who developed lung cancer and 395 matched never-smoking cancer-free women from the prospective Shanghai Women's Health Study with 15,353 metabolic features quantified in pre-diagnostic plasma using liquid chromatography high-resolution mass spectrometry. Recognizing that metabolites often correlate and seldom act independently in biological processes, we utilized a weighted correlation network analysis to agnostically construct 28 network modules of correlated metabolites. Using conditional logistic regression models, we assessed the associations for both metabolic network modules and individual metabolic features with lung cancer, accounting for multiple testing using a false discovery rate (FDR) < 0.20. We identified a network module of 121 features inversely associated with all lung cancer (p = .001, FDR = 0.028) and lung adenocarcinoma (p = .002, FDR = 0.056), where lyso-glycerophospholipids played a key role driving these associations. Another module of 440 features was inversely associated with lung adenocarcinoma (p = .014, FDR = 0.196). Individual metabolites within these network modules were enriched in biological pathways linked to oxidative stress, and energy metabolism. These pathways have been implicated in previous metabolomics studies involving populations exposed to known lung cancer risk factors such as traffic-related air pollution and polycyclic aromatic hydrocarbons. Our results suggest that untargeted plasma metabolomics could provide novel insights into the etiology and risk factors of lung cancer among never-smokers.

Prenatal Exposure to Air Pollutants Associated with Allergic Diseases in Children: Which Pollutant, When Exposure, and What Disease? A Systematic Review and Meta-analysis.

This systematic review aims to identify the association between prenatal exposure to air pollutants and allergic diseases in children, focusing on specific pollutants, timing of exposure, and associated diseases. We searched PubMed, Scopus, and Web of Science for English articles until May 1, 2023, examining maternal exposure to outdoor air pollutants (PM1, PM2.5, PM10, NO, NO2, SO2, CO, and O3) during pregnancy and child allergic diseases (atopic dermatitis (AD), food allergy (FA),asthma (AT)and allergic rhinitis (AR)/hay fever (HF)). The final 38 eligible studies were included in the meta-analysis. Exposure to PM2.5 and NO2 during pregnancy was associated with the risk of childhood AD, with pooled ORs of 1.34 (95% confidence interval (CI), 1.10-1.63) and 1.10 (95%CI, 1.05-1.15) per 10µg/m3 increase, respectively. Maternal exposure to PM1, PM2.5, and NO2 with a 10µg/m3 increase posed a risk for AT, with pooled ORs of 1.34 (95%CI, 1.17-1.54), 1.11 (95%CI, 1.05-1.18), and 1.07 (95%CI, 1.02-1.12), respectively. An increased risk of HF was observed for PM2.5 and NO2 with a 10µg/m3 increase, with ORs of 1.36 (95%CI, 1.17-1.58) and 1.26 (95%CI, 1.08-1.48), respectively. Traffic-related air pollutants (TRAP), particularly PM2.5 and NO2, throughout pregnancy, pose a pervasive risk for childhood allergies. Different pollutants may induce diverse allergic diseases in children across varying perinatal periods. AT is more likely to be induced by outdoor air pollutants as a health outcome. More research is needed to explore links between air pollution and airway-derived food allergies.

Perinatal exposure to traffic related air pollutants and the risk of infection in the first six months of life: a cohort study from a low-middle income country.

There is limited study from low-and-middle income countries on the effect of perinatal exposure to air pollution and the risk of infection in infant. We assessed the association between perinatal exposure to traffic related air pollution and the risk of infection in infant during their first six months of life. A prospective cohort study was performed in Jakarta, March 2016-September 2020 among 298 mother-infant pairs. PM2.5, soot, NOx, and NO2 concentrations were assessed using land use regression models (LUR) at individual level. Repeated interviewer-administered questionnaires were used to obtain data on infection at 1, 2, 4 and 6months of age. The infections were categorized as upper respiratory tract (runny nose, cough, wheezing or shortness of breath), lower respiratory tract (pneumonia, bronchiolitis) or gastrointestinal tract infection. Logistic regression models adjusted for covariates were used to assess the association between perinatal exposure to air pollution and the risk of infection in the first six months of life. The average concentrations of PM2.5 and NO2 were much higher than the WHO recommended levels. Upper respiratory tract infections (URTI) were much more common in the first six months of life than diagnosed lower respiratory tract or gastro-intestinal infections (35.6%, 3.5% and 5.8% respectively). Perinatal exposure to PM2.5 and soot suggested increase cumulative risk of upper respiratory tract infection (URTI) in the first 6months of life per IQR increase with adjusted OR of 1.50 (95% CI 0.91; 2.47) and 1.14 (95% CI 0.79; 1.64), respectively. Soot was significantly associated with the risk of URTI at 4-6months age interval (aOR of 1.45, 95%CI 1.02; 2.09). All air pollutants were also positively associated with lower respiratory tract infection, but all CIs include unity because of relatively small samples. Adjusted odds ratios for gastrointestinal infections were close to unity. Our study adds to the evidence that perinatal exposure to fine particles is associated with respiratory tract infection in infants in a low-middle income country.

The effects of urban green space and road proximity to indoor traffic-related PM2.5, NO2, and BC exposure in inner-city schools.

Since there are known adverse health impacts of traffic-related air pollution, while at the same time there are potential health benefits from greenness, it is important to examine more closely the impacts of these factors on indoor air quality in urban schools. This study investigates the association of road proximity and urban greenness to indoor traffic-related fine particulate matter (PM2.5), nitrogen dioxide (NO2), and black carbon (BC) in inner-city schools. PM2.5, NO2, and BC were measured indoors at 74 schools and outdoors at a central urban over a 10-year period. Seasonal urban greenness was estimated using the Normalized Difference Vegetation Index (NDVI) with 270 and 1230 m buffers. The associations between indoor traffic-related air pollution and road proximity and greenness were investigated with mixed-effects models. The analysis showed linear decays of indoor traffic-related PM2.5, NO2, and BC by 60%, 35%, and 22%, respectively for schools located at a greater distance from major roads. The results further showed that surrounding school greenness at 270 m buffer was significantly associated (p < 0.05) with lower indoor traffic-related PM2.5: -0.068 (95% CI: -0.124, -0.013), NO2: -0.139 (95% CI: -0.185, -0.092), and BC: -0.060 (95% CI: -0.115, -0.005). These associations were stronger for surrounding greenness at a greater distance from the schools (buffer 1230 m) PM2.5: -0.101 (95% CI: -0.156, -0.046) NO2: -0.122 (95% CI: -0.169, -0.075) BC: -0.080 (95% CI: -0.136, -0.026). These inverse associations were stronger after fully adjusting for regional pollution and meteorological conditions. More than 90% of children under the age of 15 worldwide are exposed to elevated air pollution levels exceeding the WHO's guidelines. The study investigates the impact that urban infrastructure and greenness, in particular green areas and road proximity, have on indoor exposures to traffic-related PM2.5, NO2, and BC in inner-city schools. By examining a 10-year period the study provides insights for air quality management, into how road proximity and greenness at different buffers from the school locations can affect indoor exposure.

Exposure to outdoor ambient air toxics and risk of breast cancer: The multiethnic cohort

BackgroundA growing literature has reported associations between traffic-related air pollution and breast cancer, however there are fewer investigations into specific ambient agents and any putative risk of breast cancer development, particularly studies occurring in populations residing in higher pollution areas such as Los Angeles. ObjectivesTo estimate breast cancer risks related to ambient air toxics exposure at residential addresses. MethodsWe examined the relationships between ambient air toxics and breast cancer risk in the Multiethnic Cohort among 48,665 California female participants followed for cancer from 2003 through 2013. We obtained exposure data on chemicals acting as endocrine disruptors or mammary gland carcinogens from the National-Scale Air Toxics Assessment. Cox proportional hazards models were used to estimate breast cancer risk per one interquartile range (IQR) increase in air toxics exposure lagged by 5-years. Stratified analyses were conducted by race, ethnicity, and hormone receptor types. ResultsAmong all women, increased risks of invasive breast cancer were observed with toxicants related to industries [1,1,2,2-tetrachloroethane (hazard ratio [HR] = 4.22, 95% confidence interval [95% CI] 3.18–5.60), ethylene dichloride (HR = 2.81, 95% CI 2.20–3.59), and vinyl chloride (HR = 2.27, 95% CI 1.81, 2.85); these 3 agents were correlated (r2 = 0.45–0.77)]. Agents related to gasoline production or combustion were related to increased breast cancer risk [benzene (HR = 1.32, 95% CI 1.24, 1.41), ethylbenzene (HR = 1.20, 95% CI 1.13–1.28), toluene (HR = 1.29, 95% CI 1.20–1.38), naphthalene (HR = 1.11, 95% CI 1.02–2.22), acrolein (HR = 2.26, 95% CI 1.92, 2.65)]. Higher hazard ratios were observed in African Americans and Whites compared to other racial and ethnic groups (p-heterogeneity <0.05 for traffic-related air toxics, acrolein, and vinyl acetate). ConclusionsOur findings suggest that specific toxic air pollutants may be associated with increase breast cancer risk.

EAACI guidelines on environmental science for allergy and asthma: The impact of short-term exposure to outdoor air pollutants on asthma-related outcomes and recommendations for mitigation measures.

The EAACI Guidelines on the impact of short-term exposure to outdoor pollutants on asthma-related outcomes provide recommendations for prevention, patient care and mitigation in a framework supporting rational decisions for healthcare professionals and patients to individualize and improve asthma management and for policymakers and regulators as an evidence-informed reference to help setting legally binding standards and goals for outdoor air quality at international, national and local levels. The Guideline was developed using the GRADE approach and evaluated outdoor pollutants referenced in the current Air Quality Guideline of the World Health Organization as single or mixed pollutants and outdoor pesticides. Short-term exposure to all pollutants evaluated increases the risk of asthma-related adverse outcomes, especially hospital admissions and emergency department visits (moderate certainty of evidence at specific lag days). There is limited evidence for the impact of traffic-related air pollution and outdoor pesticides exposure as well as for the interventions to reduce emissions. Due to the quality of evidence, conditional recommendations were formulated for all pollutants and for the interventions reducing outdoor air pollution. Asthma management counselled by the current EAACI guidelines can improve asthma-related outcomes but global measures for clean air are needed to achieve significant impact.

Persistent DNA Methylation Changes across the First Year of Life and Prenatal Exposure in a Canadian Prospective Birth Study.

Evidence suggests that prenatal air pollution exposure alters DNA methylation (DNAm), which could go on to affect long-term health. It remains unclear whether DNAm alterations present at birth persist through early life. Identifying persistent DNAm changes would provide greater insight into the molecular mechanisms contributing to the association of prenatal air pollution exposure with atopic diseases. This study investigated DNAm differences associated with prenatal nitrogen dioxide () exposure (a surrogate measure of traffic-related air pollution) at birth and 1 y of age and examined their role in atopic disease. We focused on regions showing persistent DNAm differences from birth to 1 y of age and regions uniquely associated with postnatal exposure. Microarrays measured DNAm at birth and at 1 y of age for an atopy-enriched subset of Canadian Health Infant Longitudinal Development (CHILD) study participants. Individual and regional DNAm differences associated with prenatal () were identified, and their persistence at age 1 y were investigated using linear mixed effects models (). Postnatal-specific DNAm differences () were isolated, and their association with in the first year of life was examined. Causal mediation investigated whether DNAm differences mediated associations between and age 1 y atopy or wheeze. Analyses were repeated using biological sex-stratified data. At birth (), 18 regions of DNAm were associated with , with several annotated to HOX genes. Some of these regions were specifically identified in males (), but not females (). The effect of prenatal across CpGs within altered regions persisted at 1 y of age. No significant mediation effects were identified. Sex-stratified analyses identified postnatal-specific DNAm alterations. Regional cord blood DNAm differences associated with prenatal persisted through at least the first year of life in CHILD participants. Some differences may represent sex-specific alterations, but replication in larger cohorts is needed. The early postnatal period remained a sensitive window to DNAm perturbations. https://doi.org/10.1289/EHP13034.

The effects of genetic and modifiable risk factors on brain regions vulnerable to ageing and disease

We have previously identified a network of higher-order brain regions particularly vulnerable to the ageing process, schizophrenia and Alzheimer’s disease. However, it remains unknown what the genetic influences on this fragile brain network are, and whether it can be altered by the most common modifiable risk factors for dementia. Here, in ~40,000 UK Biobank participants, we first show significant genome-wide associations between this brain network and seven genetic clusters implicated in cardiovascular deaths, schizophrenia, Alzheimer’s and Parkinson’s disease, and with the two antigens of the XG blood group located in the pseudoautosomal region of the sex chromosomes. We further reveal that the most deleterious modifiable risk factors for this vulnerable brain network are diabetes, nitrogen dioxide – a proxy for traffic-related air pollution – and alcohol intake frequency. The extent of these associations was uncovered by examining these modifiable risk factors in a single model to assess the unique contribution of each on the vulnerable brain network, above and beyond the dominating effects of age and sex. These results provide a comprehensive picture of the role played by genetic and modifiable risk factors on these fragile parts of the brain.

Nitrogen dioxide exposure, attentional function, and working memory in children from 4 to 8 years: Periods of susceptibility from pregnancy to childhood

BackgroundAir pollution exposure during pregnancy and childhood has been linked to executive function impairment in children, however, very few studies have assessed these two exposure periods jointly to identify susceptible periods of exposure. We sought to identify potential periods of susceptibility of nitrogen dioxide (NO2) exposure from conception to childhood on attentional function and working memory in school-aged children. MethodsWithin the Spanish INMA Project, we estimated residential daily NO2 exposures during pregnancy and up to 6 years of childhood using land use regression models (n = 1,703). We assessed attentional function at 4–6 years and 6–8 years, using the Conners Kiddie Continuous Performance Test and the Attention Network Test, respectively, and working memory at 6–8 years, using the N-back task. We used distributed lag non-linear models to assess the periods of susceptibility of each outcome, adjusting for potential confounders and correcting for multiple testing. We also stratified all models by sex. ResultsHigher exposure to NO2 between 1.3 and 1.6 years of age was associated with higher hit reaction time standard error (HRT-SE) (0.14 ms (95 % CI 0.05; 0.22) per 10 μg/m3 increase in NO2) and between 1.5 and 2.2 years of age with more omission errors (1.02 (95 % CI 1.01; 1.03) of the attentional function test at 4–6 years. Higher exposure to NO2 between 0.3 and 2.2 years was associated with higher HRT-SE (10.61 ms (95 % CI 3.46; 17.75) at 6–8 years only in boys. We found no associations between exposure to NO2 and working memory at 6–8 years. ConclusionOur findings suggest that NO2 exposure during the first two years of life is associated with poorer attentional function in children from 4 to 8 years of age, especially in boys. These findings highlight the importance of exploring long-term effects of traffic-related air pollution exposure in older age groups.

Surfactants and Microbial Aerosol of Urban Particulate Matter (PM10) in Kuala Lumpur City Centre

Surfactants in the atmosphere potentially influence the global climate and may affect human health. This study aims to determine the compositions of surfactants extracted from urban particulate matter (PM10) and motor vehicle exhaust soot. In addition, microbial aerosol was also determined. A high-volume air sampler (HVAS) has been used to collect PM10 samples in Kuala Lumpur urban area. Meanwhile, the vehicle exhaust soot was collected randomly from the exhaust pipes of various types of diesel and petrol vehicles, using a soft brush during dry days. The concentration of anionic surfactants as Methylene Blue Active Substances (MBAS) was determined by the colorimetric method using a UV-Vis Spectrophotometer. The presence of microorganisms such as bacteria and fungi were investigated by colony count. In addition, the correlation between surfactants and traffic-related air pollutants has also been investigated. Results revealed that the average concentration of MBAS in particulate matter is 107.68 ± 7.91 µgm-3. Diesel vehicles demonstrated higher surfactant concentration in exhaust particulate matter with an average value of 0.227 ± 0.006 µmolg-1 compared to petrol vehicles (0.146 ± 0.003 µmolg-1). Based on this study, various mitigation procedures can be implemented to reduce the impacts of PM and exhaust soot for a better future.

Integrating traffic pollution dispersion into spatiotemporal NO2 prediction

Accurately predicting ambient NO2 concentrations has great public health importance, as traffic-related air pollution is of major concern in urban areas. In this study, we present a novel approach incorporating traffic contribution to NO2 prediction in a fine-scale spatiotemporal model. We used nationally available traffic estimate dataset in a scalable dispersion model, Research LINE source dispersion model (RLINE). RLINE estimates then served as an additional input for a validated spatiotemporal pollution modeling approach. Our analysis uses measurement data collected by the Multi-Ethnic Study of Atherosclerosis and Air Pollution in the greater Los Angeles area between 2006 and 2009. We predicted road-type-specific annual average daily traffic (AADT) on road segments via national-level spatial regression models with nearest-neighbor Gaussian processes (spNNGP); the spNNGP models were trained based on over half a million point-level traffic volume measurements nationwide. AADT estimates on all highways were combined with meteorological data in RLINE models. We evaluated two strategies to integrate RLINE estimates into spatiotemporal NO2 models: 1) incorporating RLINE estimates as a space-only covariate and, 2) as a spatiotemporal covariate. The results showed that integrating the RLINE estimates as a space-only covariate improved overall cross-validation R2 from 0.83 to 0.84, and root mean squared error (RMSE) from 3.58 to 3.48 ppb. Incorporating the estimates as a spatiotemporal covariate resulted in similar model improvement. The improvement of our spatiotemporal model was more profound in roadside monitors alongside highways, with R2 increasing from 0.56 to 0.66 and RMSE decreasing from 3.52 to 3.11 ppb. The observed improvement indicates that the RLINE estimates enhanced the model's predictive capabilities for roadside NO2 concentration gradients even after considering a comprehensive list of geographic covariates including the distance to roads. Our proposed modeling framework can be generalized to improve high-resolution prediction of NO2 exposure – especially near major roads in the U.S.

Confounders Effecting Quality of Life of COPD Patients in European Union: A Systematic Review

Introduction: Chronic Obstructive Pulmonary Disease (COPD) is a respiratory disease characterized by restriction in expiratory airflow. It is among one of the major causes of illness and death globally. COPD causes severe negative effects on physical and mental health. It has a drastic effect upon the health-related quality of life of patients. Numerous factors contribute towards morbidity of COPD that include smoking, obesity, air pollutants and comorbid conditions (cardiovascular diseases, diabetes mellitus, arterial hypertension, infections). Aims and Objectives: The current systematic review was conducted with the aim to determine the health-related quality of life of COPD patients as well as the confounders of quality of life. Methodology: A systematic review was conducted of 22 studies. The electronic databases used to search the articles were Pubmed, Scopus, Science Direct, ProQuest, Web of Science. Total 1880 studies were found, out of which only 22 studies met the inclusion criteria. All the studies included are within 2017-2022. Patients met inclusion criteria have less than 70% FEV1/FVC ratio and diagnosis of patients was according to the GOLD staging system. Majority study design were observational, some were cross sectional, experimental and randomized clinical trials. Mean age of patients observed was 40-85 years. To assess the quality of life of COPD patient specific questionnaires has been used like SGRQ, CAT, CCQ, EQ-5D-5L.  Results: Included studies shows that the quality of life of COPD is compromised physically as well as mentally. It is due to less physical activities, smoking habits, psychological issues, comorbidities like diabetes mellitus, cardiovascular diseases, arterial hypertension. Conclusion: All the studies concluded that COPD patients diagnosed on basis of GOLD criteria and their quality of life is assessed via disease specific questionnaires that majorly includes SGRQ, CAT, CCQ, EQ-5D-5L. And it shows that quality of life of COPD decreases overall. However, the major confounders of reduced quality of life in COPD patients were: Smoking, raised BMI, high cholesterol, Depression/ anxiety, traffic related air pollutants, malnutrition and co-morbid conditions such as hypertension, asthma, anemia and diabetes mellitus.

History of pollutant adjuvants in respiratory allergy.

Combined exposures to allergens and air pollutants emerged as a topic of concern in scientific circles by the 1980's, when it became clear that parallel increases in respiratory allergies and traffic-related air pollution had been occurring during the 20th century. Although historically there has been a tendency to treat exposure-related symptoms as either allergic or toxicologic in nature, cross-interactions have since been established between the two modalities. For example, exposure to selected air pollutants in concert with a given allergen can increase the likelihood that an individual will become sensitized to that allergen, strongly suggesting that the pollutant acted as an adjuvant. Although not a review of underlying mechanisms, the purpose of this mini-review is to highlight the potential significance of co-exposure to adjuvant chemicals in predicting allergic sensitization in the respiratory tract. The current discussion emphasizes the upper airway as a model for respiratory challenge studies, the results of which may be applicable-not only to allergic rhinitis-but also to conjunctivitis and asthma.

Assessment of seasonal variations in vehicular emissions at traffic intersections in Ibadan using AERMOD dispersion model

AbstractAfrican cities grapple with urban air pollution from traffic‐related air pollutants (TRAPs). This study investigated TRAPs concentration variations at traffic intersections (TIs) in Ibadan, Nigeria. AERMOD model was employed to examine TRAPs dispersion at 25 selected TIs, considered as volume sources. Seasonal concentration distributions of six pollutants (CO, NO2, SO2, TVOCs, PM2.5, and PM10) were determined using meteorological, topographical, and pollutants’ emission rates in AERMOD. Estimated peak concentrations of the studied pollutants were generally higher in the rainy season than dry season, surpassing the air quality standards set by World Health Organization (WHO) and Nigeria's National Environmental Standards and Regulations Enforcement Agency (NESREA) during the rainy and dry seasons except SO2 (24 h) concentration which did not exceed the NESREA standard. This study highlighted TIs as significant contributors to air quality degradation in both seasons studied in Ibadan and showed AERMOD's suitability for air dispersion studies.

Airborne Exposure to Pollutants and Mental Health: A Review with Implications for United States Veterans.

Inhalation of airborne pollutants in the natural and built environment is ubiquitous; yet, exposures are different across a lifespan and unique to individuals. Here, we reviewed the connections between mental health outcomes from airborne pollutant exposures, the biological inflammatory mechanisms, and provide future directions for researchers and policy makers. The current state of knowledge is discussed on associations between mental health outcomes and Clean Air Act criteria pollutants, traffic-related air pollutants, pesticides, heavy metals, jet fuel, and burn pits. Although associations between airborne pollutants and negative physical health outcomes have been a topic of previous investigations, work highlighting associations between exposures and psychological health is only starting to emerge. Research on criteria pollutants and mental health outcomes has the most robust results to date, followed by traffic-related air pollutants, and then pesticides. In contrast, scarce mental health research has been conducted on exposure to heavy metals, jet fuel, and burn pits. Specific cohorts of individuals, such as United States military members and in-turn, Veterans, often have unique histories of exposures, including service-related exposures to aircraft (e.g. jet fuels) and burn pits. Research focused on Veterans and other individuals with an increased likelihood of exposure and higher vulnerability to negative mental health outcomes is needed. Future research will facilitate knowledge aimed at both prevention and intervention to improve physical and mental health among military personnel, Veterans, and other at-risk individuals.

Different Impacts of Traffic-Related Air Pollution on Early-Onset and Late-Onset Asthma.

Early-onset asthma (EOA) and late-onset asthma (LOA) are two distinct phenotypes. Air pollution has been associated with an increase in poorer asthma outcomes. The objective of this study was to examine the effects of traffic-related air pollution (TRAP) on asthma outcomes in EOA and LOA patients. A cross-sectional study was conducted on 675 asthma patients (LOA: 415) recruited from a major medical center in Taiwan. The land-use regression (LUR) model was used to estimate the level of exposure to PM10, PM2.5, NO2, and O3 on an individual level. We investigated the association between TRAP and asthma outcomes in EOA and LOA patients, stratified by allergic sensitization status, using a regression approach. An increase in PM10 was associated with younger age of onset, increased asthma duration, and decreased lung function in EOA patients (p<0.05). An increase in PM10 was associated with older age of onset, and decreased asthma duration, eosinophil count, and Asthma Control Test (ACT) score in LOA patients. An increase in PM2.5 was associated with younger age of onset, increased asthma duration, decreased eosinophil count, and lung function in EOA patients (p<0.05). An increase in PM2.5 was associated with decreased lung function and ACT score in LOA patients. An increase in NO2 was associated with increased eosinophil count and decreased lung function in EOA patients (p<0.05). An increase in O3 was associated with decreased lung function in LOA patients (p<0.05). In addition, associations of TRAP with age of onset and eosinophil counts were mainly observed in both EOA and LOA patients with allergic sensitization, and an association with ACT was mainly observed in LOA patients without allergic sensitization. The impact of TRAP on age of onset, eosinophil count, and lung function in EOA patients, and ACT in LOA patients, was affected by the status of allergic sensitization.

Roadway construction as a natural experiment to examine air pollution impacts on infant health

Traffic-related air pollution (TRAP) poses a significant public health risk that is associated with adverse birth outcomes. Large roadway infrastructure projects present a natural experiment to examine how resulting congestion change is associated with adverse birth outcomes for nearby populations. This study is designed to examine the influence of living close to a roadway before, during, and after a construction project using a difference-in-differences design. We integrated data on all large roadway construction projects (defined as widening of existing roads, building new roads, improving bridges, installing intelligent transportation systems, improving intersections, and installing or upgrading traffic signals) in Texas from 2007 to 2016 with Vital Statistic data for all births with residential addresses within 1 km of construction projects. Our outcomes included term low birth weight, term birth weight, preterm birth, and very preterm birth. Using a difference-in-differences design, we included births within 3 years of construction start and 2 years of construction end. In our main model, the exposed group is limited to pregnant individuals residing within 300 m of a construction project, and the control group includes those living within 300–1000 m from a project. We used regression models to estimate the influence of construction on infant health. We included 1360 large roadway construction projects linked to 408,979 births. During construction, we found that the odds of term low birth weight increased by 19% (95% CI: 1.05, 1.36). However, we saw little evidence of an association for other birth outcomes. Contrary to our hypothesis of decreased TRAP after construction ends, we did not observe consistent improvements post-construction for pregnant individuals living within 300 m. Continued consideration of the influence of traffic congestion programs on birth outcomes is necessary to inform future policy decisions.

Causal Mediation of Neighborhood-Level Pediatric Hospitalization Inequities.

Population-wide racial inequities in child health outcomes are well documented. Less is known about causal pathways linking inequities and social, economic, and environmental exposures. Here, we sought to estimate the total inequities in population-level hospitalization rates and determine how much is mediated by place-based exposures and community characteristics. We employed a population-wide, neighborhood-level study that included youth <18 years hospitalized between July 1, 2016 and June 30, 2022. We defined a causal directed acyclic graph a priori to estimate the mediating pathways by which marginalized population composition causes census tract-level hospitalization rates. We used negative binomial regression models to estimate hospitalization rate inequities and how much of these inequities were mediated indirectly through place-based social, economic, and environmental exposures. We analyzed 50 719 hospitalizations experienced by 28 390 patients. We calculated census tract-level hospitalization rates per 1000 children, which ranged from 10.9 to 143.0 (median 45.1; interquartile range 34.5 to 60.1) across included tracts. For every 10% increase in the marginalized population, the tract-level hospitalization rate increased by 6.2% (95% confidence interval: 4.5 to 8.0). After adjustment for tract-level community material deprivation, crime risk, English usage, housing tenure, family composition, hospital access, greenspace, traffic-related air pollution, and housing conditions, no inequity remained (0.2%, 95% confidence interval: -2.2 to 2.7). Results differed when considering subsets of asthma, type 1 diabetes, sickle cell anemia, and psychiatric disorders. Our findings provide additional evidence supporting structural racism as a significant root cause of inequities in child health outcomes, including outcomes at the population level.