Exploring the triple burden of social disadvantage, mobility poverty, and exposure to traffic-related air pollution.

Understanding the relationships between ultrafine particle (UFP) exposure, socioeconomic status (SES), and sustainable transportation accessibility in Toronto, Canada is crucial for promoting public health, addressing environmental justice, and ensuring transportation equity. We conducted a large-scale mobile measurement campaign and employed a gradient boost model to generate exposure surfaces using land use, built environment, and meteorological conditions. The Ontario Marginalization Index was used to quantify various indicators of social disadvantage for Toronto's neighborhoods. Our findings reveal that people in socioeconomically disadvantaged areas experience elevated UFP exposures. We highlight significant disparities in accessing sustainable transportation, particularly in areas with higher ethnic concentrations. When factoring in daily mobility, UFP exposure disparities in disadvantaged populations are further exacerbated. Furthermore, individuals who do not generate emissions themselves are consistently exposed to higher UFPs, with active transportation users experiencing the highest UFP exposures both at home and at activity locations. Finally, we proposed a novel index, the Community Prioritization Index (CPI), incorporating three indicators, including air quality, social disadvantage, and sustainable transportation. This index identifies neighborhoods experiencing a triple burden, often situated near major infrastructure hubs with high diesel truck activity and lacking greenspace, marking them as high-priority areas for policy action and targeted interventions.

Communication between healthcare providers and communicatively-vulnerable patients with associated health outcomes: A scoping review of knowledge syntheses.

OBJECTIVE: Summarize literature on provider-patient communication linked to health outcomes in communicatively-vulnerable patient populations. METHODS: Scoping review of reviews: systematically searched six databases. INCLUSION CRITERIA: systematic searches and syntheses of literature; one or more providers and communicatively-vulnerable patients; synchronous in-person communication; intermediate or health outcome linked to communication. RESULTS: The search yielded 14,615 citations; 47 reviews - with wide range of providers, communication vulnerabilities, communication practices, and health outcomes - met inclusion criteria. Methodology included qualitative, quantitative, and mixed approaches. Quality ranged from very low to high. Six categories of communication practices linked to health outcomes were identified: 1) motivation-based; 2) accommodation of language, culture, gender, sexual identity, and other concordance with the patient; 3) cultural adaptations of interventions; 4) use of interpreters; 5) other provider-patient communication practices; 6) patient communication practices. CONCLUSION: Communication practices were studied in a wide range of providers, with common themes regarding best practices. A unique finding is the role of the patient's communication practices. The specificity of communication practices studied is heterogeneous, with many reviews providing insufficient details. PRACTICE IMPLICATIONS: Motivation-based practices and culturally- and linguistically-appropriate care have impacts on patient outcomes across a range of settings with different professions and communicatively-vulnerable groups.

Predicting spatial variations in annual average outdoor ultrafine particle concentrations in Montreal and Toronto, Canada: Integrating land use regression and deep learning models.

BACKGROUND: Concentrations of outdoor ultrafine particles (UFP; <0.1 µm) and black carbon (BC) can vary greatly within cities and long-term exposures to these pollutants have been associated with a variety of adverse health outcomes. OBJECTIVE: This study integrated multiple approaches to develop new models to estimate within-city spatial variations in annual median (i.e. average) outdoor UFP and BC concentrations as well as mean UFP size in Canada's two largest cities, Montreal and Toronto. METHODS: We conducted year-long mobile monitoring campaigns in each city that included evenings and weekends. We developed generalized additive models trained on land use parameters and deep Convolutional Neural Network (CNN) models trained on satellite-view images. Using predictions from these models, we developed final combined models. RESULTS: In Toronto, the median observed UFP concentration, UFP size, and BC concentration values were 16,172pt/cm3, 33.7 nm, and 1225 ng/m3, respectively. In Montreal, the median observed UFP concentration, UFP size, and BC concentration values were 14,702pt/cm3, 29.7 nm, and 1060 ng/m3, respectively. For all pollutants in both cities, the proportion of spatial variation explained (i.e., R2) was slightly greater (1-2 percentage points) for the combined models than the generalized additive models and a greater (approximately 10 percentage points) than the deep CNN models. The Toronto combined model R2 values in the test set were 0.73, 0.55, and 0.61 for UFP concentrations, UFP size, and BC concentration, respectively. The Montreal combined model R2 values were 0.60, 0.49, and 0.60 for UFP concentration, UFP size, and BC concentration models respectively. For each pollutant, predictions from the combined, deep CNN, and generalized additive models were highly correlated with each other and differences between models were explored in sensitivity analyses. CONCLUSION: Predictions from these models are available to support future epidemiological research examining long-term health impacts of outdoor UFPs and BC.

Prediction of Short-Term Ultrafine Particle Exposures Using Real-Time Street-Level Images Paired with Air Quality Measurements.

Within-city ultrafine particle (UFP) concentrations vary sharply since they are influenced by various factors. We developed prediction models for short-term UFP exposures using street-level images collected by a camera installed on a vehicle rooftop, paired with air quality measurements conducted during a large-scale mobile monitoring campaign in Toronto, Canada. Convolutional neural network models were trained to extract traffic and built environment features from images. These features, along with regional air quality and meteorology data were used to predict short-term UFP concentration as a continuous and categorical variable. A gradient boost model for UFP as a continuous variable achieved R2 = 0.66 and RMSE = 9391.8#/cm3 (mean values for 10-fold cross-validation). The model predicting categorical UFP achieved accuracies for "Low" and "High" UFP of 77 and 70%, respectively. The presence of trucks and other traffic parameters were associated with higher UFPs, and the spatial distribution of elevated short-term UFP followed the distribution of single-unit trucks. This study demonstrates that pictures captured on urban streets, associated with regional air quality and meteorology, can adequately predict short-term UFP exposure. Capturing the spatial distribution of high-frequency short-term UFP spikes in urban areas provides crucial information for the management of near-road air pollution hot spots.

Patient characteristics associated with enrolment under voluntary programs implemented within fee-for-service systems in British Columbia and Quebec: a cross-sectional study.

BACKGROUND: There is a paucity of information on patient characteristics associated with enrolment under voluntary programs (e.g. incentive payments) implemented within fee-for-service systems. We explored patient characteristics associated with enrolment under these programs in British Columbia and Quebec. METHODS: We used linked administrative data and a cross-sectional design to compare people aged 40 years or more enrolled under voluntary programs to those who were eligible but not enrolled. We examined 2 programs in Quebec (enrolment of vulnerable patients with qualifying conditions [implemented in 2003] and enrolment of the general population [2009]) and 3 in BC (Chronic disease incentive [2003], Complex care incentive [2007] and enrolment of the general population [A GP for Me, 2013]). We used logistic regression to estimate the odds of enrolment by neighbourhood income, rural versus urban residence, previous treatment for mental illness, previous treatment for substance use disorder and use of health care services before program implementation, controlling for characteristics linked to program eligibility. RESULTS: In Quebec, we identified 1 569 010 people eligible for the vulnerable enrolment program (of whom 505 869 [32.2%] were enrolled within the first 2 yr of program implementation) and 2 394 923 for the general enrolment program (of whom 352 380 [14.7%] were enrolled within the first 2 yr). In BC, we identified 133 589 people eligible for the Chronic disease incentive, 47 619 for the Complex care incentive and 1 349 428 for A GP for Me; of these, 60 764 (45.5%), 28 273 (59.4%) and 1 066 714 (79.0%), respectively, were enrolled within the first 2 years. The odds of enrolment were higher in higher-income neighbourhoods for programs without enrolment criteria (adjusted odds ratio [OR] comparing highest to lowest quintiles 1.21 [95% confidence interval (CI) 1.20-1.23] in Quebec and 1.67 [95% CI 1.64-1.69] in BC) but were similar across neighbourhood income quintiles for programs with health-related eligibility criteria. The odds of enrolment by urban versus rural location varied by program. People treated for substance use disorders had lower odds of enrolment in all programs (adjusted OR 0.60-0.72). Compared to people eligible but not enrolled, those enrolled had similar or higher numbers of primary care visits and longitudinal continuity of care in the year before enrolment. INTERPRETATION: People living in lower-income neighbourhoods and those treated for substance use disorders were less likely than people in higher-income neighbourhoods and those not treated for such disorders to be enrolled in programs without health-related eligibility criteria. Other strategies are needed to promote equitable access to primary care.

Aryl hydrocarbon receptor deficiency causes the development of chronic obstructive pulmonary disease through the integration of multiple pathogenic mechanisms.

Emphysema, a component of chronic obstructive pulmonary disease (COPD), is characterized by irreversible alveolar destruction that results in a progressive decline in lung function. This alveolar destruction is caused by cigarette smoke, the most important risk factor for COPD. Only 15%-20% of smokers develop COPD, suggesting that unknown factors contribute to disease pathogenesis. We postulate that the aryl hydrocarbon receptor (AHR), a receptor/transcription factor highly expressed in the lungs, may be a new susceptibility factor whose expression protects against COPD. Here, we report that Ahr-deficient mice chronically exposed to cigarette smoke develop airspace enlargement concomitant with a decline in lung function. Chronic cigarette smoke exposure also increased cleaved caspase-3, lowered SOD2 expression, and altered MMP9 and TIMP-1 levels in Ahr-deficient mice. We also show that people with COPD have reduced expression of pulmonary and systemic AHR, with systemic AHR mRNA levels positively correlating with lung function. Systemic AHR was also lower in never-smokers with COPD. Thus, AHR expression protects against the development of COPD by controlling interrelated mechanisms involved in the pathogenesis of this disease. This study identifies the AHR as a new, central player in the homeostatic maintenance of lung health, providing a foundation for the AHR as a novel therapeutic target and/or predictive biomarker in chronic lung disease.

Glyphosate but not Roundup® harms earthworms (Eisenia fetida).

Glyphosate is the active ingredient in Roundup® formulations. While multiple studies have documented the toxicity, environmental persistence, and tendency to spread for glyphosate and Roundup®, few studies have compared the toxicity of glyphosate-based formulations to the toxicity of pure glyphosate for soil invertebrates, which contact both the herbicide and the formulations. Hundreds of formulations exist; their inert ingredients are confidential; and glyphosate persists in our food, water, and soil. In this experiment, we held glyphosate type and concentration constant, varying only formulation. Using Roundup Ready-to-Use III®, Roundup Super Concentrate®, and pure glyphosate, we delivered 26.3 mg glyphosate in the form of isopropylamine salt per kg of soil to compost worms (Eisenia fetida). We found that worms living in soil spiked with pure glyphosate lost 14.8-25.9% of their biomass and survived a stress test for 22.2-33.3% less time than worms living in uncontaminated soil. Worms living in soil spiked with Roundup Ready-to-Use III® and Roundup Super Concentrate® did not lose body mass and survived the stress test as well as worms living in uncontaminated soil. No contaminant affected soil microbial or fungal biomass over the 40-day period of this experiment. We suggest that the nitrates and phosphates in the formulations offset the toxic effects of glyphosate by spurring microbial growth and speeding glyphosate degradation. We also found a 26.5-41.3% reduction in fungal biomass across all treatments over the course of this experiment, suggesting that the worms consumed fungi and spores.

HB-EGF Synthesized by CD4 T Cells Modulates Allergic Airway Eosinophilia by Regulating IL-5 Synthesis.

CD4 T cells express the epidermal growth factor (EGF) receptor ligand, heparin-binding EGF (HB-EGF), with no defined immuno-pathophysiological function. Therefore, we wished to elucidate the function of HB-EGF synthesized by CD4 T cells in the context of allergic pulmonary inflammation and the asthma surrogate, airway hyperresponsiveness, in a murine acute model of asthma. In this study, we show how knocking out HB-EGF expression in CD4 T cells in vivo attenuates IL-5 synthesis in the lung that is accompanied by diminished eosinophilic inflammation and airway hyperresponsiveness. HB-EGF coimmunoprecipitates with the transcriptional repressor B cell lymphoma 6 (Bcl-6) in CD4 T cells. Knocking out HB-EGF in CD4 T cells resulted in increased Bcl-6 binding to the IL-5 gene and decreased IL-5 mRNA expression. Thus, these findings suggest an immunoregulatory function for intrinsic HB-EGF expressed by CD4 T cells in TH2 inflammation and airway dysfunction by modulating IL-5 expression via binding to and inhibiting the repressive function of Bcl-6.

March1 E3 Ubiquitin Ligase Modulates Features of Allergic Asthma in an Ovalbumin-Induced Mouse Model of Lung Inflammation.

Membrane-associated RING-CH-1 (March1) is a member of the March family of E3 ubiquitin ligases. March1 downregulates cell surface expression of MHC II and CD86 by targeting them to lysosomal degradation. Given the key roles of MHC class II and CD86 in T cell activation and to get further insights into the development of allergic inflammation, we asked whether March1 deficiency exacerbates or attenuates features of allergic asthma in mice. Herein, we used an acute model of allergy to compare the asthmatic phenotype of March1-deficient and -sufficient mice immunized with ovalbumin (OVA) and later challenged by intranasal instillation of OVA in the lungs. We found that eosinophilic inflammation in airways and lung tissue was similar between WT and March1-/- allergic mice, whereas neutrophilic inflammation was significant only in March1-/- mice. Airway hyperresponsiveness as well as levels of IFN-γ, IL-13, IL-6, and IL-10 was lower in the lungs of asthmatic March1-/- mice compared to WT, whereas lung levels of TNF-α, IL-4, and IL-5 were not significantly different. Interestingly, in the serum, levels of total and ova-specific IgE were reduced in March1-deficient mice as compared to WT mice. Taken together, our results demonstrate a role of March1 E3 ubiquitin ligase in modulating allergic responses.

Human airway branch variation and chronic obstructive pulmonary disease.

Susceptibility to chronic obstructive pulmonary disease (COPD) beyond cigarette smoking is incompletely understood, although several genetic variants associated with COPD are known to regulate airway branch development. We demonstrate that in vivo central airway branch variants are present in 26.5% of the general population, are unchanged over 10 y, and exhibit strong familial aggregation. The most common airway branch variant is associated with COPD in two cohorts (n = 5,054), with greater central airway bifurcation density, and with emphysema throughout the lung. The second most common airway branch variant is associated with COPD among smokers, with narrower airway lumens in all lobes, and with genetic polymorphisms within the FGF10 gene. We conclude that central airway branch variation, readily detected by computed tomography, is a biomarker of widely altered lung structure with a genetic basis and represents a COPD susceptibility factor.