UNASSIGNED: Epidemic Thunderstorm asthma (TA) is a serious public health threat with a potential to overwhelm health systems. Being the first documented incidence in Ghana, we sought to determine whether the chronic respiratory risk factors for the development of TA as identified in other countries were similar or different from that in Ghana.
UNASSIGNED: A matched case-control study involving 41 cases and 82 controls was conducted in two conveniently selected health facilities in the Ashanti Region of Ghana.
UNASSIGNED: Data were collected from pre-existing patient records and included general demography, a history of allergies and a history of asthma. A chi-square and multiple logistic regression analysis were conducted to identify risk factors for the development of TA.
UNASSIGNED: Overall, 53.7 % of the TA cases and 7.3 % of controls had a previous history of asthma (AOR = 4.53 p = 0.064, 95 % CI = 0.918-22.365). Also, 29.3 % of the cases and 1.2 % of the controls had a previous history of allergies (AOR = 12.48 p = 0.05, 95 % CI = 0.919-169.305).
UNASSIGNED: A previous history of allergy was a significant risk factor for TA. A previous history of asthma though associated with TA, was not a significant risk factor for its development. The recognition and awareness of risk factors for TA, by clinicians and health managers, is essential for health education, case management and preparation for the surge capacity occasioned by the event.

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Pollen allergies, such as allergic rhinitis, are triggered by exposure to airborne pollen. They are a considerable global health burden, with their numbers expected to rise in the coming decades due to the advent of climate change and air pollution. The relationships that exist between pollens, meteorological, and environmental conditions are complex due to a lack of clarity on the nature and conditions associated with these interactions; therefore, it is challenging to describe their direct impacts on allergenic potential clearly. This article attempts to review evidence pertaining to the possible influence of meteorological factors and air pollutants on the allergic potential of pollen by studying the interactions that pollen undergoes, from its inception to atmospheric traversal to human exposure. This study classifies the evidence based on the nature of these interactions as physical, chemical, source, and biological, thereby simplifying the complexities in describing these interactions. Physical conditions facilitating pollen rupturing for tree, grass, and weed pollen, along with their mechanisms, are studied. The effects of pollen exposure to air pollutants and their impact on pollen allergenic potential are presented along with the possible outcomes following these interactions, such as pollen fragmentation (SPP generation), deposition of particulate matter on pollen exine, and modification of protein levels in-situ of pollen. This study also delves into evidence on plant-based (source and biological) interactions, which could indirectly influence the allergic potential of pollen. The current state of knowledge, open questions, and a brief overview of future research directions are outlined and discussed. We suggest that future studies should utilise a multi-disciplinary approach to better understand this complex system of pollen interactions that occur in nature.

The objective of this article is to review recent literature on the implications of extreme weather events such as thunderstorms, wildfires, tropical cyclones, freshwater flooding, and temperature extremes in relationship to asthma symptoms. Several studies have shown worsening of asthma symptoms with thunderstorms, wildfires, tropical cyclones, freshwater flooding, and temperature extremes. In particular, thunderstorm asthma can be exacerbated by certain factors such as temperature, precipitation, and allergen sensitization. Therefore, it is imperative that the allergy and immunology community be aware of the health effects associated with these extreme weather events in order to educate patients and engage in mitigation strategies.

There have been 26 epidemic thunderstorm asthma (ETSA) events worldwide, with Melbourne at the epicentre of ETSA with 7 recorded events, and in 2016 experienced the deadliest ETSA event ever recorded. Health services and emergency departments were overwhelmed with thousands requiring medical care for acute asthma and 10 people died.
This multidisciplinary study was conducted across various health and science departments with the aim of improving our collective understanding of the mechanism behind ETSA.
This study involved time-resolved analysis of atmospheric sampling of the air for pollen and fungal spores, and intact and ruptured pollen compared with different weather parameters, pollution levels and clinical asthma presentations.
Time-resolved pollen and fungal spore data collected by Deakin AirWATCH Burwood, underwent 3-h analysis, to better reflect the \'before\', \'during\' and \'after\' ETSA time points, on the days leading up to and following the Melbourne 2016 event. Linear correlations were conducted with atmospheric pollution data provided by the Environment Protection Authority (EPA) of Victoria, weather data sourced from Bureau of Meteorology (BOM) and clinical asthma presentation data from the Victorian Agency for Health Information (VAHI) of Department of Health.
Counts of ruptured grass pollen grains increased 250% when the thunderstorm outflow reached Burwood. Increased PM10, high relative humidity, decreased temperature and low ozone concentrations observed in the storm outflow were correlated with increased levels of ruptured grass pollen. In particular, high ozone levels observed 6 h prior to this ETSA event may be a critical early indicator of impending ETSA event, since high ozone levels have been linked to increasing pollen allergen content and reducing pollen integrity, which may in turn contribute to enhanced pollen rupture.
The findings presented in this article highlight the importance of including ruptured pollen and time-resolved analysis to forecast ETSA events and thus save lives.

Climate change is a key environmental factor for allergic respiratory diseases, especially in childhood. This review describes the influences of climate change on childhood asthma considering the factors acting directly, indirectly and with their amplifying interactions. Recent findings on the direct effects of temperature and weather changes, as well as the influences of climate change on air pollution, allergens, biocontaminants and their interplays, are discussed herein. The review also focusses on the impact of climate change on biodiversity loss and on migration status as a model to study environmental effects on childhood asthma onset and progression. Adaptation and mitigation strategies are urgently needed to prevent further respiratory diseases and human health damage in general, especially in younger and future generations.

There is clear evidence that climate change is occurring as there has been an acceleration of global temperatures since the mid-nineteenth century along with rising atmospheric carbon dioxide levels. It has been proposed that one of the most significant consequences of climate change on human health could be the impact on aeroallergens. Evidence from around globe has pointed to longer and more abundant pollen season associated with global warming. Additional studies have also suggested increased pollen allergenicity due to air pollution.

The climate crisis poses a major challenge to human health as well as the healthcare system and threatens to jeopardize the medical progress made in recent decades. However, addressing climate change may also be the greatest opportunity for global health in the 21st century. The climate crisis and its consequences, such as rising temperatures, forest fires, floods, droughts, and changes in the quality and quantity of food and water, directly and indirectly affect human physical and mental health. More intense and frequent heat waves and declining air quality have been shown to increase all-cause mortality, especially among the most vulnerable. Climate warming alters existing ecosystems and favors biological invasions by species that better tolerate heat and drought. Pathogen profiles are changing, and the transmission and spread of vector-borne diseases are increasing. The spread of neophytes in Europe, such as ragweed, is creating new pollen sources that increase allergen exposure for allergy sufferers. In addition, the overall milder weather, especially in combination with air pollution and increased CO2 levels, is changing the production and allergenicity of pollen. The phenomenon of thunderstorm asthma is also occurring more frequently. In view of the increasing prevalence of allergic diseases due to climate change, early causal immunomodulatory therapy is therefore all the more important. During a climate consultation, patients can receive individual advice on climate adaptation and resilience and the benefits of CO2 reduction-for their own and the planet\'s health. Almost 5% of all greenhouse gas emissions in Europe come from the healthcare sector. It thus has a central responsibility for a climate-neutral and sustainable transformation.

Despite making up a significant proportion of airborne allergens, the relationship between fungal spores and asthma is not fully explored. Only 80 taxa of fungi have so far been observed to exacerbate respiratory presentations, with Cladosporium spp., Aspergillus spp., Penicillium spp., and Alternaria spp. found to comprise the predominant allergenic airborne spores. Fungal spores have been found in indoor environments, such as hospitals and housing due to poor ventilation. Meanwhile, outdoor fungal spores exhibit greater diversity, and higher abundance and have been associated with hospitalizations from acute asthma presentations. In addition, fungal spores may be the underlying, and perhaps the \"missing link\", factor influencing the heightened rate of asthma presentations during epidemic thunderstorm asthma events. To improve our knowledge gap on fungal spores, airborne allergen monitoring must be improved to include not only dominant allergenic fungi but also provide real-time data to accurately and quickly warn the general public. Such data will help prevent future asthma exacerbations and thus save lives. In this review, we examine the health risks of prominent allergenic fungal taxa, the factors influencing spore dispersal and distribution, and why improvements should be made to current sampling methods for public health and wellbeing.

Grass pollens have been identified as mediators of respiratory distress, capable of exacerbating respiratory diseases including epidemic thunderstorm asthma (ETSA). It is hypothesised that during thunderstorms, grass pollen grains swell to absorb atmospheric water, rupture, and release internal protein content to the atmosphere. The inhalation of atmospheric grass pollen proteins results in deadly ETSA events. We sought to identify the underlying cellular mechanisms that may contribute towards the severity of ETSA in temperate climates using Timothy grass (Phleum pratense). Respiratory cells exposed to Timothy grass pollen protein extract (PPE) caused cells to undergo hypoxia ultimately triggering the subcellular re-organisation of F-actin from the peri junctional belt to cytoplasmic fibre assembly traversing the cell body. This change in actin configuration coincided with the spatial reorganisation of microtubules and importantly, decreased cell compressibility specifically at the cell centre. Further to this, we find that the pollen-induced reorganisation of the actin cytoskeleton prompting secretion of the pro-inflammatory cytokine, interleukin-8. In addition, the loss of peri-junctional actin following exposure to pollen proteins was accompanied by the release of epithelial transmembrane protein, E-cadherin from cell-cell junctions resulting in a decrease in epithelial barrier integrity. We demonstrate that Timothy grass pollen regulates F-actin dynamics and E-cadherin localisation in respiratory cells to mediate cell-cell junctional integrity highlighting a possible molecular pathway underpinning ETSA events.