Addressing overdose risks and fatalities in public bathrooms: insights from the development of a Safer Bathroom Toolkit in British Columbia, Canada.

SETTING: In British Columbia (BC), over 11,000 people have died of an overdose since 2016. Recently, an all-party standing committee on health tabled a report identifying several gaps in BC's overdose response. Chief among these is the inequitable distribution of supervised consumption and overdose prevention services across BC and barriers to accessing services that are currently available. In this context, public bathrooms continue to act as consumption spaces and contribute to overdose-related risks and fatalities. INTERVENTION: The Safer Bathroom project sought to address long-standing policy and practice gaps by developing a toolkit to improve bathroom overdose prevention and response. Activities included a literature review and cross-sectoral, province-wide consultation (Fall 2021), the creation and launch of the Safer Bathroom Toolkit (Fall 2022), and knowledge transfer activities (ongoing). OUTCOMES: The toolkit meets four objectives. First, it provides a bathroom safety checklist that helps identify and, most importantly, mitigate safety risks. Second, it offers organizational guidance on developing a bathroom safety policy and procedure. Third, it includes practical resources such as staff training material and signs that communicate bathroom safety messages in a non-stigmatizing manner. Finally, it identifies bathroom architecture and design features that can increase or decrease overdose-related risks. IMPLICATIONS: The Safer Bathroom Toolkit is a highly comprehensive resource developed in response to the overdose crisis. However, significant reporting, research, policy, and practice gaps remain. This paper concludes with an overview of recommendations for advancing overdose prevention and response efforts within and beyond the bathroom context.

RéSUMé: LIEU: En Colombie-Britannique (C.-B.), plus de 11 000 personnes sont décédées d'une surdose depuis 2016. Un comité multipartite en santé a récemment déposé un rapport identifiant plusieurs écarts dans la réponse du gouvernement de la C.-B. face aux surdoses. La distribution inéquitable des services de consommation supervisée et de prévention des surdoses ainsi que les barrières d'accès aux services qui sont disponibles constituent un écart important. Dans ce contexte, les toilettes publiques servent d'espaces de consommation et contribuent au risque de surdoses ainsi qu'aux surdoses mortelles. INTERVENTION: Le projet visant à améliorer la sécurité dans les toilettes publiques avait pour but de répondre à des lacunes de longue date en matière de politiques et de pratiques et ce, en proposant des outils pour prévenir les surdoses et faciliter les réponses aux surdoses en cas d'urgence. Les activités réalisées dans le cadre de ce projet incluent une revue de la littérature et une consultation intersectorielle à l'échelle provinciale (automne 2021), la création et le lancement d'une trousse d'outils (automne 2022), et les activités de transfert des connaissances (en cours). RéSULTATS: La trousse d'outils répond à quatre objectifs. Premièrement, elle contient une liste de vérification permettant d'identifier, et surtout, de diminuer les risques à la sécurité dans les toilettes publiques. Deuxièmement, elle offre des directives aux organisations qui souhaitent développer une politique et une procédure pour améliorer la sécurité dans leurs toilettes publiques. Troisièmement, elle propose des ressources pratiques pour la formation du personnel et des affiches permettant de communiquer des messages ayant pour but de promouvoir la sécurité sans toutefois stigmatiser. Finalement, elle décrit les caractéristiques architecturales pouvant augmenter ou diminuer les risques associés aux surdoses par le biais d'une fiche d'information. CONSéQUENCES: La trousse d'outils que nous avons développée contient des ressources complètes qui répondent à la crise des surdoses. Toutefois, des lacunes importantes en matière de surveillance, de recherche, de politiques, et de pratiques demeurent. Nous proposons certaines recommandations pour améliorer la réponse aux surdoses et les efforts de prévention dans les toilettes publiques et de façon plus large en conclusion de cet article.

Reduced presynaptic vesicle stores mediate cellular and network plasticity defects in an early-stage mouse model of Alzheimer's disease.

BACKGROUND: Identifying effective strategies to prevent memory loss in AD has eluded researchers to date, and likely reflects insufficient understanding of early pathogenic mechanisms directly affecting memory encoding. As synaptic loss best correlates with memory loss in AD, refocusing efforts to identify factors driving synaptic impairments may provide the critical insight needed to advance the field. In this study, we reveal a previously undescribed cascade of events underlying pre and postsynaptic hippocampal signaling deficits linked to cognitive decline in AD. These profound alterations in synaptic plasticity, intracellular Ca2+ signaling, and network propagation are observed in 3-4 month old 3xTg-AD mice, an age which does not yet show overt histopathology or major behavioral deficits. METHODS: In this study, we examined hippocampal synaptic structure and function from the ultrastructural level to the network level using a range of techniques including electron microscopy (EM), patch clamp and field potential electrophysiology, synaptic immunolabeling, spine morphology analyses, 2-photon Ca2+ imaging, and voltage-sensitive dye-based imaging of hippocampal network function in 3-4 month old 3xTg-AD and age/background strain control mice. RESULTS: In 3xTg-AD mice, short-term plasticity at the CA1-CA3 Schaffer collateral synapse is profoundly impaired; this has broader implications for setting long-term plasticity thresholds. Alterations in spontaneous vesicle release and paired-pulse facilitation implicated presynaptic signaling abnormalities, and EM analysis revealed a reduction in the ready-releasable and reserve pools of presynaptic vesicles in CA3 terminals; this is an entirely new finding in the field. Concurrently, increased synaptically-evoked Ca2+ in CA1 spines triggered by LTP-inducing tetani is further enhanced during PTP and E-LTP epochs, and is accompanied by impaired synaptic structure and spine morphology. Notably, vesicle stores, synaptic structure and short-term plasticity are restored by normalizing intracellular Ca2+ signaling in the AD mice. CONCLUSIONS: These findings suggest the Ca2+ dyshomeostasis within synaptic compartments has an early and fundamental role in driving synaptic pathophysiology in early stages of AD, and may thus reflect a foundational disease feature driving later cognitive impairment. The overall significance is the identification of previously unidentified defects in pre and postsynaptic compartments affecting synaptic vesicle stores, synaptic plasticity, and network propagation, which directly impact memory encoding.

Proximity to major roadways is a risk factor for airway hyper-responsiveness in adults.

BACKGROUND: Proximity to major roads is reported to be associated with asthma and airway hyper-responsiveness in children. Similar studies using objective measurements in adults are not available in Canada. OBJECTIVE: To test the hypothesis that adult asthmatic patients who live close to major roads and highways in an urban environment are at a risk of moderate to severe airway hyper-responsiveness. METHODS: Airway responsiveness was determined using methacholine bronchial provocation (PC(20)) tests in a cohort of 2625 patients who attended an outpatient clinic in Hamilton, Ontario. Patient addresses were geocoded in a geographic information system to determine proximity to major roads and highways. Multivariate linear and multinomial regression analyses were used to assess whether proximity to roads was a risk factor for airway hyper-responsiveness as measured by PC(20) methacholine. RESULTS: Patients who lived within 200 m of a major road had increased odds (OR 1.38 [95% CI 1.04 to 1.85]) of having moderate airway hyperresponsiveness (0.25 mg/mL 16 mg/mL). Spatial analysis also revealed that the majority of patients with severe airway hyper-responsiveness lived within the urban core of the city while those with moderate to mild hyper-responsiveness were also dispersed in rural areas. CONCLUSIONS: In an adult population of patients attending an outpatient respiratory clinic in Hamilton, living close to major roadways was associated with an increased risk of moderate airway hyper-responsiveness. This correlation suggests that exposure to traffic emissions may provoke the pathology of airway hyper-responsiveness leading to variable airflow obstruction.