No abstract

The European Union (EU) has mechanisms in place to support countries when an environmental emergency strikes and it deploys experts to assist the local community. These experts may find themselves in a chaotic situation, in which local and national authorities are overwhelmed. Collating the necessary evidence from scattered sources to conduct a robust risk assessment is a major challenge and deployed experts may not have access to the necessary technical expertise.Therefore, the European Multiple Environmental Threats Emergency Network (EMETNET) project is building a simple, efficient and robust methodology to enable the rapid risk assessment (RRA) of environmental emergencies. The RRA, which will be delivered to the European Commission (EC), presents an overview of potential and actual health and environmental impacts of the event. A network of risk assessors is being built to carry out this RRA and provide back-office support to deployed experts, enabling them to have rapid access to information and expertise. EMETNET builds on existing methodologies for the RRA of environmental emergencies, in particular, on a methodology developed for serious cross-border chemical health threats.The EMETNET methodology will support the selection of experts and assets deployed to affected regions and provide a snapshot assessment to experts en route to disaster zones. It will aid defensible decision-making, communication, planning and risk management. Furthermore, it will ensure a harmonised understanding of the associated health, environmental and cross-sectoral impacts of an environmental emergency.

Allergic airways disease (AAD) is a collective term for respiratory disorders that can be exacerbated upon exposure to airborne allergens. The contribution of fungal allergens to the pathogenesis of AAD has become well established over recent years and can be present in the air we breathe as bioaerosols. Understanding the mechanisms allergy to fungal bioaerosols can help to better manage symptoms and conditions, reducing the burden of disease. We conducted a comprehensive review to collate the current understanding of mechanisms involved in the allergic response to fungal bioaerosols in airway epithelia. To be included in the final analysis, studies were compared to defined inclusion/exclusion criteria, relevant data was extracted, and each paper was assessed using a quality scoring tool. The search string provided 440 initial results with 60 studies selected for final analysis. 120 potential target mechanisms were identified within the selected studies and 17 were identified in more than 5 studies. The major pathways identified in allergic response include 1) a role for proteases and the activation of the PAR2 receptor, 2) release of IL33, 3) EGFR pathway and mucin expression, and 4) a skewing towards a Th2 profile promoting eosinophil recruitment. However, there was conflicting evidence when comparing results from individual studies. Thus, further research is required to better understand which fungi/fungal components drive the allergic response. Funding: This work has been funded under the NIHR Health Protection Research Unit for Environmental Exposures and Health with Imperial College London

Quantifying the burden of disease from exposure to poor indoor air pollution can support policy development. In England, there is current regulatory and public attention on the health implications of residential exposure to formaldehyde, damp and mould. However, there is scarce information on these health impacts at the population scale. As such, we assessed the burden of key respiratory diseases from residential formaldehyde, damp and/or mould for the English population aged 0–14 and 15–49. We obtained data on the percentage of dwellings affected by damp and/or mould from the English Housing Survey and estimated the distribution of residential formaldehyde concentrations (annual average (μg/m3)) by pooling data from monitoring studies conducted in England. Exposures were combined with epidemiological relationships and national health data to estimate Population Attributable Fractions (PAFs), disease incidence, and Disability Adjusted Life Years (DALYs) lost associated with residential formaldehyde or damp and/or mould exposure in England. We made estimates for the year 2019 but also looked back several years in time. Exposure to formaldehyde was associated with approximately 4000 new cases of childhood asthma (~800 DALYs lost) in 2019, though the estimates were sensitive to the placement of the lower exposure threshold. Exposure to damp and/or mould was associated with approximately 5000 new cases of asthma (~2200 DALYs) and approximately 8500 lower respiratory infections (~600 DALYs) among children and adults in 2019, though the PAFs were unequally distributed across dwellings based on income and ethnicity. Alternative data sources suggest that the percentage of dwellings affected by damp and/or mould may even be higher, resulting in a possible 3–8-fold greater number of cases and DALYs. Our assessment emphasizes a potential respiratory health burden in England associated with residential formaldehyde as well as damp and/or mould, further highlighting the public health importance of good indoor air quality and good quality housing.

Allergic airway disease (AAD) is a collective term for respiratory disorders that can be exacerbated upon exposure to airborne allergens, including fungi and other air pollutants. Fungi are of particular interest as they are present in both outdoor and indoor air and are associated with asthma and allergy. A recent literature review identified key pathways contributing to the allergic responses to fungal allergens. However, due to the heterogeneity of models and methods used, it is not clear whether there are common or specific pathways induced by different fungi/fungal components. Air-liquid interface (ALI) culture was used to induce differentiation of nasal (RPMI 2650), bronchial (HBEC3-KT, BEAS-2B, Calu-3) and small airways (A549) epithelial cells into a columnar stratified epithelium with cilia, goblet cells, and the formation of tight junctions. Cultures were harvested at 0, 7, 14, 21 and 28 days, and the expression of molecular markers of basal, ciliated and mucus producing cells were assessed with reverse-transcription quantitative PCR (RT-qPCR). Different cell lines produce subtly different differentiated models, with downregulation of basal (undifferentiated) cell markers and upregulation of markers of ciliated and mucus producing cells from day 7. While no ciliated cells were observed in any of the differentiated cell lines, mucus was produced in some. The differentiation of primary cell lines at ALI, and expression of genes of interest (including known fungal receptors and genes identified in driving fungal allergy) were also measured to inform selection of appropriate model(s) to better understand the allergenic response to fungi/fungal components.