OBJECTIVE: Traffic-related ultrafine particle pollution near highways is associated with adverse health. Reducing exposure by use of portable air purifiers in homes is one approach to reducing this risk. However, the reaction of residents to having air purifiers in homes is not well studied.
METHODS: Within the framework of our randomized crossover trial of air purifiers in homes near a major highway, we collected data about participants\' use and reactions to air purifiers using questionnaires at their 30-day and 90-day home visits, recorded electricity consumption using HOBO monitors, and conducted structured interviews with participants.
RESULTS: Nearly all 150 participants reported running the air purifiers virtually 24 h every day in both their living room and their bedroom in the prior month. The units\' HOBO electricity use, from a subset of 45 participants, supported the participants\' responses from the questionnaire. Approximately 80% of participants reported setting their air purifier on the medium setting. Tolerance to air purifier noise increased significantly between the 30-day and 90-day home visits, with approximately two thirds reporting not being bothered at all by the noise. The qualitative interviews in a subset of 26 participants yielded consistent responses to those from the questionnaires. Size of unit, airflow, and energy consumption were additional concerns that emerged during the interviews.
CONCLUSIONS: Results from the questionnaires, HOBO data, and structured interviews all suggest participants had positive reactions towards the presence of in-home APs, and therefore may be receptive to using air purifiers in their homes on a regular basis.
BACKGROUND: ClinicalTrials.gov, NCT04279249 . Registered 09 October 2019.

Worldwide, there is an increasing uptake of traffic management interventions aimed at reducing the impact of traffic related air pollution on public health. However, the evidence base linking the proposed changes with the resulting improvements in air quality is lacking. In this paper we present data from a micro-network of low-cost PM10 samplers collected from an isolated urban centre (Auckland, New Zealand). The data was then analysed using a new combination of analytical methods aimed to identify the composition and hence, the source of pollution. Whilst across the three sites mass concentration of PM10 and black carbon were similar, Raman spectroscopy successfully identified variations in the soot composition at different sites, enabling some particulate matter to be linked to diesel vehicle emissions. A mass reconstruction approach proved useful in determining that the airshed is well-mixed and also highlighted the impacts of urban design on recorded concentrations. The results show that networks of low-cost sensors, combined with the range of analytical techniques used here can help policymakers test the efficacy of interventions and management strategies designed to combat the burden of air pollution on public health.

BACKGROUND: The discriminatory and racist policy of historical redlining in the United States during the 1930s played a role in perpetuating contemporary environmental health disparities.
OBJECTIVE: Our objectives were to determine associations between home and school pollutant exposure (fine particulate matter [PM2.5], NO2) and respiratory outcomes (Composite Asthma Severity Index, lung function) among school-aged children with asthma and examine whether associations differed between children who resided and/or attended school in historically redlined compared to non-redlined neighborhoods.
METHODS: Children ages 6 to 17 with moderate-to-severe asthma (N = 240) from 9 US cities were included. Combined home and school exposure to PM2.5 and NO2 was calculated based on geospatially assessed monthly averaged outdoor pollutant concentrations. Repeated measures of Composite Asthma Severity Index and lung function were collected.
RESULTS: Overall, 37.5% of children resided and/or attended schools in historically redlined neighborhoods. Children in historically redlined neighborhoods had greater exposure to NO2 (median: 15.4 vs 12.1 parts per billion) and closer distance to a highway (median: 0.86 vs 1.23 km), compared to those in non-redlined neighborhoods (P < .01). Overall, PM2.5 was not associated with asthma severity or lung function. However, among children in redlined neighborhoods, higher PM2.5 was associated with worse asthma severity (P < .005). No association was observed between pollutants and lung function or asthma severity among children in non-redlined neighborhoods (P > .005).
CONCLUSIONS: Our findings highlight the significance of historical redlining and current environmental health disparities among school-aged children with asthma, specifically, the environmental injustice of PM2.5 exposure and its associations with respiratory health.

Vehicle-emitted fine particulate matter (PM2.5) has been associated with significant health outcomes and environmental risks. This study estimates the contribution of traffic-related exhaust emissions (TREE) to observed PM2.5 using a novel factorization framework. Specifically, co-measured nitrogen oxides (NOx) concentrations served as a marker of vehicle-tailpipe emissions and were integrated into the optimization of a Non-negative Matrix Factorization (NMF) analysis to guide the factor extraction. The novel TREE-NMF approach was applied to long-term (2012-2019) PM2.5 observations from air quality monitoring (AQM) stations in two urban areas. The extracted TREE factor was evaluated against co-measured black carbon (BC) and PM2.5 species to which the TREE-NMF optimization was blind. The contribution of the TREE factor to the observed PM2.5 concentrations at an AQM station from the first location showed close agreement (R2=0.79) with monitored BC data. In the second location, a comparison of the extracted TREE factor with measurements at a nearby Surface PARTiculate mAtter Network (SPARTAN) station revealed moderate correlations with PM2.5 species commonly associated with fuel combustion, and a good linear regression fit with measured equivalent BC concentrations. The estimated concentrations of the TREE factor at the second location accounted for 7-11 % of the observed PM2.5 in the AQM stations. Moreover, analysis of specific days known to be characterized by little traffic emissions suggested that approximately 60-78 % of the traffic-related PM2.5 concentrations could be attributed to particulate traffic-exhaust emissions. The methodology applied in this study holds great potential in areas with limited monitoring of PM2.5 speciation, in particular BC, and its results could be valuable for both future environmental health research, regional radiative forcing estimates, and promulgation of tailored regulations for traffic-related air pollution abatement.

The evidence associating traffic-related air pollution (TRAP) with allergic asthma is growing, but the underlying mechanisms for this association remain unclear. The airway epithelium is the primary tissue exposed to TRAP, hence understanding its interactions with TRAP and allergen is important. Diesel exhaust (DE), a paradigm of TRAP, consists of particulate matter (PM) and gases. Modern diesel engines often have catalytic diesel particulate filters to reduce PM output, but these may increase gaseous concentrations, and their benefits on human health cannot be assumed. We conducted a randomized, double-blinded, crossover study using our unique in vivo human exposure system to investigate the effects of DE and allergen co-exposure, with or without particle depletion as a proxy for catalytic diesel particulate filters, on the airway epithelial transcriptome. Participants were exposed for 2 h before an allergen inhalation challenge, with each receiving filtered air and saline (FA-S), filtered air and allergen (FA-A), DE and allergen (DE-A), or particle-depleted DE and allergen (PDDE-A), over four different occasions, each separated by a 4-week washout period. Endobronchial brushings were collected 48 h after each exposure, and total RNA was sequenced. Differentially expressed genes (DEGs) were identified using DESeq2, followed by GO enrichment and pathway analysis. FA-A, DE-A, and PDDE-A exposures significantly modulated genes relative to FA-S, with 462 unique DEGs identified. FA-A uniquely modulated the highest number (↑178, ↓155), followed by DE-A (↑44, ↓23), and then PDDE-A exposure (↑15, ↓2); 6 DEGs (↑4, ↓2) were modulated by all three conditions. Exposure to PDDE-A resulted in modulation of 285 DEGs compared to DE-A exposure, further revealing 26 biological process GO terms, including \"cellular response to chemokine\" and \"inflammatory response\". The transcriptional epithelial response to diesel exhaust and allergen co-exposure is enriched in inflammatory mediators, the pattern of which is altered upon particle depletion.

BACKGROUND: Ambient air pollution has been linked to postpartum depression. However, few studies have investigated the effects of traffic-related NOx on postpartum depression and whether any pregnancy-related factors might increase susceptibility.
OBJECTIVE: To evaluate the association between traffic-related NOx and postpartum depressive and anxiety symptoms, and effect modification by pregnancy-related hypertension.
METHODS: This study included 453 predominantly low-income Hispanic/Latina women in the MADRES cohort. Daily traffic-related NOx concentrations by road class were estimated using the California LINE-source dispersion model (CALINE4) at participants\' residential locations and averaged across pregnancy. Postpartum depressive and anxiety symptoms were evaluated by a validated questionnaire (Postpartum Distress Measure, PDM) at 1, 3, 6 and 12 months postpartum. Multivariate linear regressions were performed to estimate the associations at each timepoint. Interaction terms were added to the linear models to assess effect modification by hypertensive disorders of pregnancy (HDPs). Repeated measurement analyses were conducted by using mixed effect models.
RESULTS: We found prenatal traffic-related NOx was associated with increased PDM scores. Specifically, mothers exposed to an IQR (0.22 ppb) increase in NOx from major roads had 3.78% (95% CI: 0.53-7.14%) and 5.27% (95% CI: 0.33-10.45%) significantly higher 3-month and 12-month PDM scores, respectively. Similarly, in repeated measurement analyses, higher NOx from major roads was associated with 3.06% (95% CI: 0.43-5.76%) significantly higher PDM scores across the first year postpartum. Effect modification by HDPs was observed: higher freeway/highway and total NOx among mothers with HDPs were associated with significantly higher PDM scores at 12 months postpartum compared to those without HDPs.
CONCLUSIONS: This study shows that prenatal traffic-related air pollution was associated with postpartum depressive and anxiety symptoms. The study also found novel evidence of greater susceptibility among women with HDPs, which advances the understanding of the relationships between air pollution, maternal cardiometabolic health during pregnancy and postpartum mental health. Our study has potential implications for clinical intervention to mitigate the effects of traffic-related pollution on postpartum mental health disorders. The findings can also offer valuable insights into urban planning strategies concerning the implementation of emission control measures and the creation of green spaces.

BACKGROUND: Sickle cell disease (SCD) is a genetic disorder and symptoms may be sensitive to environmental stressors. Although it has been hypothesized that exposure to outdoor air pollution could trigger acute SCD events, evidence is limited.
METHODS: We obtained SCD administrative data on hospital encounters in South Carolina from 2002 to 2019. We estimated outdoor air pollutant (particulate matter<2.5 μm (PM2.5), ozone (O3), and PM2.5 elemental carbon (EC) concentrations at residential zip codes using spatio-temporal models. Using a random bi-directional, fixed-interval case-crossover study design, we investigated the relationship between air pollution exposure over 1-, 3-, 5-, 9-, and14-day periods with SCD hospital encounters.
RESULTS: We studied 8410 patients with 144,129 hospital encounters. We did not observe associations among all patients with SCD and adults for PM2.5, O3, and EC. We observed positive associations among children for 9- and 14-day EC (OR: 1.05 (95% confidence interval (CI): 1.02, 1.08) and OR: 1.05 (95% CI: 1.02, 1.09), respectively) and 9- and 14-day O3 (OR: 1.04 (95%CI: 1.00, 1.08)) for both.
CONCLUSIONS: Our findings suggest that short-term (within two-weeks) levels of EC and O3 and may be associated with SCD hospital encounters among children. Two-pollutant model results suggest that EC is more likely responsible for effects on SCD than O3. More research is needed to confirm our findings.

Urban air pollution is one of the most important environmental problems for human health and several strategies have been developed for its mitigation. The objective of this study is to assess the impact of single and combined mitigation measures on concentrations of air pollutants emitted by traffic at pedestrian level in the same urban environment. The effectiveness of different scenarios of green infrastructure (GI), the implementation of photocatalytic materials and traffic low emission zones (LEZ) are investigated, as well as several combinations of LEZ and GI. A wide set of scenarios is simulated through Computational Fluid Dynamics (CFD) modelling for two different wind directions (perpendicular (0°) and 45° wind directions). Wind flow for the BASE scenario without any measure implemented was previously evaluated using wind-tunnel measurements. Air pollutant concentrations for this scenario are compared with the results obtained from the different mitigation scenarios. Reduction of traffic emissions through LEZ is found to be the most effective single measure to improve local air quality. However, GI enhances the effects of LEZ, which makes the combination of LEZ + GI a very effective measure. The effectiveness of this combination depends on the GI layout, the intensity of emission reduction in the LEZ and the traffic diversion in streets surrounding the LEZ. These findings, in line with previous literature, suggest that the implementation of GI may increase air pollutant concentrations at pedestrian level for some cases. However, this study highlights that this negative effect on air quality can turn into positive when used in combination with reductions of local traffic emissions.

Exhaust from diesel combustion engines is an important contributor to urban air pollution and poses significant risk to human health. Diesel exhaust contains a chemical class known as nitrated polycyclic aromatic hydrocarbons (nitro-PAHs) and is enriched in 1-nitropyrene (1-NP), which has the potential to serve as a marker of diesel exhaust. The isomeric nitro-PAHs 2-nitropyrene (2-NP) and 2-nitrofluoranthene (2-NFL) are secondary pollutants arising from photochemical oxidation of pyrene and fluoranthene, respectively. Like other important air toxics, there is not extensive monitoring of nitro-PAHs, leading to gaps in knowledge about relative exposures and urban hotspots. Epiphytic moss absorbs water, nutrients, and pollutants from the atmosphere and may hold potential as an effective biomonitor for nitro-PAHs. In this study we investigate the suitability of Orthotrichum lyellii as a biomonitor of diesel exhaust by analyzing samples of the moss for 1-NP, 2-NP, and 2-NFL in the Seattle, WA metropolitan area. Samples were collected from rural parks, urban parks, residential, and commercial/industrial areas (N = 22 locations) and exhibited increasing concentrations across these land types. Sampling and laboratory method performance varied by nitro-PAH, but was generally good. We observed moderate to moderately strong correlation between 1-NP and select geographic variables, including summer normalized difference vegetation index (NDVI) within 250 m (r = -0.88, R2 = 0.77), percent impervious surface within 50 m (r = 0.83, R2 = 0.70), percent high development land use within 500 m (r = 0.77, R2 = 0.60), and distance to nearest secondary and connecting road (r = -0.75, R2 = 0.56). The relationships between 2-NP and 2-NFL and the geographic variables were generally weaker. Our results suggest O. lyellii is a promising biomonitor of diesel exhaust, specifically for 1-NP. To our knowledge this pilot study is the first to evaluate using moss concentrations of nitro-PAHs as biomonitors of diesel exhaust.

A growing body of literature has attempted to characterize how traffic-related air pollution (TRAP) affects molecular and subclinical biological processes in ways that could lead to cardiorespiratory disease. To provide a streamlined synthesis of what is known about the multiple mechanisms through which TRAP could lead to cardiorespiratory pathology, we conducted a systematic review of the epidemiological literature relating TRAP exposure to methylomic, proteomic, and metabolomic biomarkers in adult populations. Using the 139 papers that met our inclusion criteria, we identified the omic biomarkers significantly associated with short- or long-term TRAP and used these biomarkers to conduct pathway and network analyses. We considered the evidence for TRAP-related associations with biological pathways involving lipid metabolism, cellular energy production, amino acid metabolism, inflammation and immunity, coagulation, endothelial function, and oxidative stress. Our analysis suggests that an integrated multi-omics approach may provide critical new insights into the ways TRAP could lead to adverse clinical outcomes. We advocate for efforts to build a more unified approach for characterizing the dynamic and complex biological processes linking TRAP exposure and subclinical and clinical disease and highlight contemporary challenges and opportunities associated with such efforts.