Ocular allergy (OA) is a subtype of seasonal allergy that causes symptoms of itchiness, redness, swelling and irritation of the ocular surface and eyelids, often triggering allergy-induced eye rubbing and sustained inflammation for up to six months of the year during peak allergy season. These symptoms, coupled with reduced sleep quality, impaired daily productivity and decreased mood, highlight a significant yet underrepresented disease burden. Recent advances in tear-based multi-omics have enabled detailed characterisation of OA-associated biochemical changes on the ocular surface, highlighting human tears as a promising biospecimen for diagnostic biomarker and therapeutic target research. This review discusses emerging proteomic, lipidomic, metabolomic and miRNA findings comparing OA sufferers with healthy controls, and, where relevant, with comorbid conditions such as dry eye disease and keratoconus. Differential expression patterns across these analytes implicate key pathways involved in immune response, wound healing, angiogenesis, inflammation, oxidative stress and return to homeostasis on the ocular surface. By integrating these data into a stepwise model of OA biopathway activation, this review outlines candidate biomarkers and highlights methodological advances that may support translation of tear multi-omics into clinical tools for OA management.

Although associations between airborne allergens, weather conditions and respiratory health have been established, the precise mechanisms that contribute to the onset and severity of epidemic thunderstorm asthma (ETSA) events remain poorly understood. One critical area of this research lies in understanding the role of fungal spores, which have not been extensively studied for their impact on asthma exacerbations compared to pollen, as well as the influence of certain pollutants like ozone on airborne allergens, which is not well documented. This study aimed to identify the environmental parameters that influence the dispersal & distribution of airborne allergens and how these factors are associated with asthma presentations. Analysis was conducted on 475 days of data collected over a 6-year period between October-December. Using eight global negative binomial generalised linear mixed model formulations combined with a model selection approach, we analysed airborne levels of grass pollen, Alternaria spp., and Cladosporium spp. from Metropolitan Melbourne, along with weather values from the Bureau of Meteorology (precipitation, temperature, humidity, dew point, wind direction, wind speed, air pressure) and pollution values from the Environmental Protection Authority (CO, NO2, O3, SO2) to identify effects on asthma presentations from five emergency departments. Rainfall and O3 levels had significant positive relationships with number of asthma presentations, with Incidence Response Ratios of 1.074-1.088 and 1.05-1.06, respectively. High allergen levels (allergenPC1, representing overall levels of grass pollen and fungal spores) had an interactive effect with high rainfall creating positive association with asthma cases. On days of low rainfall, allergen levels had minimal impact on asthma presentations, but on days of high rainfall, there were substantially greater numbers of presentations when allergen levels were also high (e.g. a predicted four-fold increase on days with 45 mm of rain). This impact of overall allergen count highlights the role of several prominent allergens in seasonal asthma, as well as potential cross reactivity between pollen and spores. The results of this study will inform researchers of several environmental monitoring parameters that should be included in risk forecasts for ETSA to allow for a more robust and accurate detection system and help improve public health responses across Australia.

Objectives: Using high-performance liquid chromatography (HPLC), we developed and validated an in vitro assay for the quantitative determination of beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) activity, supplementing limited current methodologies to assess the efficacy of BACE1 inhibitor compounds. A hexa-histidine tagged peptide substrate of BACE1 was used as the analyte for the determination of in vitro BACE1 activity; it was validated according to ICH guidelines. Methods: The HPLC analysis was performed on the Agilent 1290 Series Infinity II UHPLC System equipped with a Phenomenex Kinetex EVO C18 (100 & times; 3 mm) 5 & micro;m column. The method was developed using a gradient programme comprising 10% aqueous acetonitrile (0.02 M TFA) to 30% aqueous acetonitrile (0.02 M TFA) for 5 min at a flow rate of 0.6 mL/min. Results: The method showed linearity over the range of 14.92 to 72 & micro;M with r2=0.9997. The accuracy of the method in terms of mean recovery ranged between 96.62 and 98.38%. The %RSD for intra- and inter-day precision was less than 5%. Two commercial inhibitors, AZD3839 and OM99-2, were used to evaluate the performance of the method at their respective IC50, resulting in inhibition of 53.46 and 50.74%, respectively. The described method addresses the void for a practical and cheap alternative to quantitatively determine the activity of BACE1 compared to current commercially available detection assays. Conclusions: We have successfully developed an HPLC method to measure the inhibitory function of two commercial inhibitors of BACE1, indicating the suitability of the method for the identification and characterisation of novel BACE1 inhibitors.

Background/Objectives: Ocular Allergy (OA) has profound effects on the quality of life (QoL) and ocular health of affected individuals. This study aimed to survey health practitioners in Australia on their knowledge and practices regarding currently available evidence-based diagnostic, treatment, and collaborative care approaches to OA. Methods: The Survey on Ocular Allergy for Health Practitioners (SOAHP), a validated tool, was distributed to various health practitioners across Australia in 2022. The survey data were analysed using descriptive statistics, Fisher's exact test, and non-parametric tests. Results: A total of 155 participants completed the survey including Allergists/Immunologists (n = 6), General Practitioners (GPs) (n = 29), Ophthalmologists (n = 11), Optometrists (n = 66) and Pharmacists (n = 43). The survey revealed strengths and weakness in health practitioner approaches to OA. In terms of diagnosis, a significant 83.2% of participants were aware that itchy eyes are the hallmark symptom of OA; however, only 67.7% were aware that histamine is what causes the itching. Further to this, 57.4% of participants did not ask about QoL in clinical practice. In terms of management, only 30.3% were aware that some topical allergy eye drops act on eosinophils, and 74.9% were aware of the indications of mast cell stabiliser use. Finally, in terms of collaborative care, 68.4% did not believe there was a clear collaborative care model in Australia. Conclusions: This study revealed patterns in health practitioner approaches to OA. As expected, Ophthalmologists and Optometrists exhibited higher awareness and implementation of evidence-based approaches, compared to GPs and Pharmacists. However, these distinct patterns are likely influenced by differences in training and clinical responsibilities. Nonetheless, all practitioner groups showed gaps in knowledge and evidence-based practices surrounding OA. Thus, educational initiatives are required to ensure best patient-centered care is achieved, with reduced burden on the healthcare system.

Grass pollen constitutes a significant public health concern in Australia, particularly for individuals with seasonal allergic rhinitis and asthma, due to its strong association with epidemic thunderstorm asthma (ETSA) events, which are getting more frequent due to climate change. The combined effects of humidity and lightning during ETSA events cause intact grass pollen to rupture and release small particles that can trigger severe asthma attacks, leading to increased hospital admissions. To help prevent this, researchers began collecting and monitoring local pollen data that contribute to ETSA warning systems. In Australia, expert pollen counters rely on Hirst-type traps, but these machines take 24 h to operate. Some modern machines have been designed to monitor pollen faster, but they are not able to determine the state of the pollen (i.e., intact or ruptured). The advent of artificial intelligence (AI) presents an opportunity to enhance pollen monitoring by accurately identifying not only pollen taxa but also the state of the pollen. Using AI to monitor ruptured pollen could improve the accuracy and efficiency of warning systems, thereby helping to prevent the severe outcomes associated with ETSA events.

Allergic rhinitis (hay fever) prevalence has increased in Australia. People with hay fever often experience many eye symptoms, especially itching. This study explores clinical correlations between tear IgE levels and ocular allergy signs in hay fever sufferers, focusing also on eyelid wiper friction damage from eye rubbing. In a cross-sectional study from November 2024 to January 2025, 16 individuals with self-reported hay fever and 17 healthy controls were recruited. Participants completed demographic and allergy-related questionnaires, including symptoms and quality of life assessments. Tear samples were analyzed for IgE and MMP-9 biomarkers. Ocular surface parameters-bulbar redness, palpebral roughness, and lid wiper epitheliopathy (LWE)-were graded. Corneal and conjunctival dendritic cells were also evaluated. Elevated tear IgE significantly correlated with self-reported hay fever, QUICK score, MiniRQLQ, eye rubbing frequency, and lower LWE grade. The hay fever group showed significantly higher LWE compared to healthy controls (p < 0.001), indicating frictional eyelid damage. ROC analysis of tear IgE yielded an AUC of 0.893 (cut-off 0.03 IU/mL; sensitivity 90%, specificity 85%). Tear IgE is a useful biomarker for ocular inflammation and may indicate friction-related eyelid damage in allergy sufferers. Incorporating LWE grading into clinical assessments of ocular allergy is recommended.

BackgroundOcular allergy (OA) is a localized subset of allergy characterized by ocular surface itchiness, redness and inflammation. Inflammation and eye-rubbing, due to allergy-associated itch, are common in OA sufferers and may trigger changes to the ocular surface biochemistry. The primary aim of this study is to assess the differences in the human tear proteome between OA sufferers and Healthy Controls (HCs) across peak allergy season and off-peak season in Victoria, Australia.Methods19 participants (14 OA sufferers, 5 HCs) aged 18–45 were recruited for this study. Participants were grouped based on allergy symptom assessment questionnaire scoring. Proteins were extracted from human tear samples and were run on an Orbitrap Mass Spectrometer. Peaks were matched to a DIA library. Data was analyzed using the software MaxQuant, Perseus and IBM SPSS.Results1267 proteins were identified in tear samples of OA sufferers and HCs. 23 proteins were differentially expressed between peak allergy season OA suffers vs HCs, and 21 were differentially expressed in off-peak season. Decreased proteins in OA sufferers related to cell structure regulation, inflammatory regulation and antimicrobial regulation. In both seasons, OA sufferers were shown to have increased expression of proteins relating to inflammation, immune responses and cellular development.ConclusionTear protein identification showed dysregulation of proteins involved in inflammation, immunity and cellular structures. Proteins relating to cellular structure may suggest a possible link between OA-associated itch and the subsequent ocular surface damage via eye-rubbing, while inflammatory and immune protein changes highlight potential diagnostic and therapeutic biomarkers of OA.

Patients with asthma experience elevated rates of mental illness. However, the molecular links underlying such lung–brain crosstalk remain ambiguous. Hypothalamic dysfunction is observed in many psychiatric disorders, particularly those with an inflammatory component due to many hypothalamic regions being unprotected by the blood–brain barrier. To gain a better insight into such neuropsychiatric sequelae, this study investigated gene expression differences in the hypothalamus following lung inflammation (asthma) induction in mice, using RNA transcriptome profiling. BALB/c mice were challenged with either bacterial lipopolysaccharide (LPS, E. coli) or ovalbumin (OVA) allergens or saline control (n = 7 per group), and lung inflammation was confirmed via histological examination of postmortem lung tissue. The majority of the hypothalamus was micro-dissected, and total RNA was extracted for sequencing. Differential expression analysis identified 31 statistically significant single genes (false discovery rate FDR5%) altered in expression following LPS exposure compared to controls; however, none were significantly changed following OVA treatment, suggesting a milder hypothalamic response. When gene sets were examined, 48 were upregulated and 8 were downregulated in both asthma groups relative to controls. REACTOME enrichment analysis suggests these gene sets are involved in signal transduction metabolism, immune response and neuroplasticity. Interestingly, we identified five altered gene sets directly associated with neurotransmitter signaling. Intriguingly, many of these altered gene sets can influence mental health and or/neuroinflammation in humans. These findings help characterize the links between asthma-induced lung inflammation and the brain and may assist in identifying relevant pathways and therapeutic targets for future intervention.

Ocular allergy (OA) is characterised by ocular surface itchiness, redness, and inflammation in response to allergen exposure. The primary aim of this study was to assess differences in the human tear metabolome and lipidome between OA and healthy controls (HCs) across peak allergy (spring–summer) and off-peak (autumn–winter) seasons in Victoria, Australia. A total of 19 participants (14 OA, 5 HCs) aged 18–45 were recruited and grouped by allergy questionnaire score. Metabolites and lipids from tear samples were analysed using mass spectrometry. Data were analysed using TraceFinder and Metaboanalyst. Metabolomics analysis showed 12 differentially expressed (DE) metabolites between those with OA and the HCs during the peak allergy season, and 24 DE metabolites were found in the off-peak season. The expression of niacinamide was upregulated in OA sufferers vs. HCs across both seasons (p ≤ 0.05). A total of 6 DE lipids were DE between those with OA and the HCs during the peak season, and 24 were DE in the off-peak season. Dysregulated metabolites affected oxidative stress, inflammation, and homeostasis across seasons, suggesting a link between OA-associated itch and ocular surface damage via eye rubbing. Tear lipidome changes were minimal between but suggested tear film destabilisation and thinning. Such metabolipodome findings may pave new and exciting ways for effective diagnostics and therapeutics for OA sufferers in the future.

Aim -To isolate bacteriophages targeting extended-spectrum beta-lactamase-producing K. pneumoniae and evaluate their effectiveness across diverse models, incorporating innovative alternatives in animal testing. Methods and results: vB_kpnS-Kpn15 was isolated from sewage sample from Thane district. It produced a clear plaques on K. pneumoniae ATCC 700603. It has a flexible, non-contractile long tail and an icosahedral head and the Siphoviridae family of viruses in the order Caudovirales matched all of its structural criteria. Sequencing of vB_kpnS-Kpn15 revealed a 48,404 bp genome. The vB_KpnS-Kpn15 genome was found to contain 50 hypothetical proteins, of which 16 were found to possess different functions. The vB_KpnS-Kpn15 was also found to possess enzymes for its DNA synthesis. It was found to be lytic for the planktonic cells of K. pneumoniae and bactericidal for up to 48 h and potentially affected established K. pneumoniae biofilms. It demonstrated a broad host range and caused lytic zones on about 46 % of K. pneumoniae multi-drug resistant strains. In an in vitro wound and burn infection model, phage vB_kpnS-Kpn15 in combination with other phages resulted in successful cell proliferation and wound healing. Based on vB_kpnS-Kpn15's lytic properties, it can be incorporated in a bacteriophage cocktail to combat ESBL strains. Conclusions: The phages isolated during this research are better candidates for phage therapy, and therefore provide new and exciting options for the successful control of antibiotic-resistant bacterial infections in the future. The utilization of animal alternative models in this study elucidates cellular proliferation and migration, underscoring its significance in screening novel drugs with potential applications in the treatment of wound and burn infections. Significance and impact of the research: The findings of this research have implications for the creation of innovative, promising strategies to treat ESBL K. pneumoniae infections.

Survey studies have played a significant role in understanding the gaps in the knowledge and practices of health practitioners. However, there have been no such survey studies on Ocular Allergy (OA). Thus, the purpose of this study was to develop and validate a survey on OA to better understand the gaps in the diagnostic, treatment, and collaborative care approaches of health practitioners in OA. The survey is titled "Survey on Ocular Allergy for Health Practitioners (SOAHP)". SOAHP was developed in a five-stage process. First, item extraction via the use of a literature review, second, face and content validity, third, a pilot study, fourth, test-retest reliability, and fifth, finalisation of the survey. 65 items under 6 domains were initially generated in the item extraction phase. Content validity was conducted on 15 experts in the field. This was conducted twice to reach consensus whereby items and domains were added, edited, kept, or removed, resulting in 50 items under 7 domains. The pilot study was conducted on 15 participants from the five relevant health practitioner fields (Allergists/Immunologists, General Practitioners (GPs), Ophthalmologists, Optometrists and Pharmacists). This altered the survey further to 40 items under 7 domains. Test-retest reliability was conducted on 25 participants from the five health practitioner fields. Reliability was moderate to almost perfect for most (97%) investigated items. The finalised survey was 40 items under 7 domains. SOAHP is the first survey created to assess diagnostic, treatment and collaborative care approaches of Allergists/Immunologists, GPs, Ophthalmologists, Optometrists and Pharmacists on OA. SOAHP will be a useful tool in clinical research on OA.

Neuroinflammation, characterised by the activation of immune cells in the central nervous system (CNS), plays a dual role in both protecting against and contributing to the progression of neurodegenerative diseases, such as Alzheimer’s disease (AD) and multiple sclerosis (MS). This review explores the role of phosphoinositide 3-kinase (PI3K), a key enzyme involved in cellular survival, proliferation, and inflammatory responses, within the context of neuroinflammation. Two PI3K isoforms of interest, PI3Kγ and PI3Kδ, are specific to the regulation of CNS cells, such as microglia, astrocytes, neurons, and oligodendrocytes, influencing pathways, such as Akt, mTOR, and NF-κB, that control cytokine production, immune cell activation, and neuroprotection. The dysregulation of PI3K signalling is implicated in chronic neuroinflammation, contributing to the exacerbation of neurodegenerative diseases. Preclinical studies show promise in targeting neuronal disorders using PI3K inhibitors, such as AS605240 (PI3Kγ) and idelalisib (PI3Kδ), which have reduced inflammation, microglial activation, and neuronal death in in vivo models of AD. However, the clinical translation of these inhibitors faces challenges, including blood–brain barrier (BBB) permeability, isoform specificity, and long-term safety concerns. This review highlights the therapeutic potential of PI3K modulation in neuroinflammatory diseases, identifying key gaps in the current research, particularly in the need for brain-penetrating and isoform-specific inhibitors. These findings underscore the importance of future research to develop targeted therapies that can effectively modulate PI3K activity and provide neuroprotection in chronic neurodegenerative disorders.

Pseudomonas aeruginosa is an aerobic Gram-negative rod-shaped bacterium with a comparatively large genome and an impressive genetic capability allowing it to grow in a variety of environments and tolerate a wide range of physical conditions. This biological flexibility enables the P. aeruginosa to cause a broad range of infections in patients with serious underlying medical conditions, and to be a principal cause of health care associated infection worldwide. The clinical manifestations of P. aeruginosa include mostly health care associated infections and community-acquired infections. P. aeruginosa possesses an array of virulence factors that counteract host defence mechanisms. It can directly damage host tissue while utilizing high levels of intrinsic and acquired antimicrobial resistance mechanisms to counter most classes of antibiotics. P. aeruginosa co-regulates multiple resistance mechanisms by perpetually moving targets poses a significant therapeutic challenge. Thus, there is an urgent need for novel approaches in the development of anti-Pseudomonas agents. Here we review the principal infections caused by P. aeruginosa and we discuss novel therapeutic options to tackle antibiotic resistance and treatment of P. aeruginosa infections that may be further developed for clinical practice.

Background : Ocular allergy (OA) is a localised subset of allergy characterised by ocular surface itchiness, redness and in fl ammation. In fl ammation and eye-rubbing, due to allergy-associated itchiness, are common in OA sufferers and may trigger changes to the ocular surface biochemistry. The primary aim of this study is to assess the differences in human tear proteome between OA sufferers and healthy controls during peak allergy season in Victoria, Australia. Methods : 31 participants (21 OA sufferers, 10 healthy controls) aged 18 – 45 were recruited for this study. Participants were grouped based on symptom assessment questionnaire scoring. Tear samples were collected via the non-invasive microcapillary fl ow technique. Extracted proteins were run on an Orbitrap Mass Spectrometer and were matched to a DIA library developed using high-pH HPLC. Data was statistically analysed using the software MaxQuant, Perseus and IBM SPSS. Results : 877 proteins were quanti fi ed in tear samples of OA sufferers and healthy controls, of which 23 showed a signi fi cant difference in expression between groups ( P < 0.05). Nine proteins showed increased expression in OA sufferers versus healthy controls, and 14 were decreased. Decreased proteins in OA sufferers related to cell structure regulation, in fl ammatory regulation and antimicrobial regulation. OA sufferers were shown to have increased expression of proteins relating to in fl ammation, immune responses and cellular development. Conclusions : Tear protein quanti fi cation showed dysregulation of proteins involved in in fl ammation, immunity and cellular structures. Proteins relating to cellular structure may suggest a possible link between OA-associated itch and the subsequent ocular surface damage via eye-rubbing, while in fl ammatory and immune protein changes highlight potential diagnostic and therapeutic biomarkers of OA.

Background: 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. Objectives: This multidisciplinary study was conducted across various health and science departments with the aim of improving our collective understanding of the mechanism behind ETSA. Design: 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. Methods: Time-resolved pollen and fungal spore data collected by Deakin Air WATCH 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. Results: 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. Conclusion: 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.

The prevalence of allergies is rising every year. For those who suffer from it, ocular inflammation and irritation can be inconvenient and unpleasant. Anti-allergy eyedrops are a readily available treatment for symptoms of ocular allergy (OA) and can help allergy sufferers regain normal function. However, the eye is a delicate organ, and multiuse eyedrops often utilise preservatives to deter microbial growth. Preservatives such as benzalkonium chloride (BAK) have been shown to induce decreased cell viability. Therefore, during a period of high localised inflammation and eye rubbing, it is important that the preservatives used in topical medicines do not contribute to the weakening of the corneal structure. This review explores ocular allergy and the thinning and protrusion of the cornea that is characteristic of the disease keratoconus (KC) and how it relates to a weakened corneal structure. It also describes the use of BAK and its documented effects on the integrity of the cornea. It was found that atopy and eye rubbing are significant risk factors for KC, and BAK can severely decrease the integrity of the corneal structure when compared to other preservatives and preservative-free alternatives.

In the aftermath of the catastrophic 2019–2020 bushfires, the corona virus disease of 2019 pandemic and recent devastating floods in New South Wales and Queensland, Australians voted for climate action in the 2022 Federal election, and a new Climate Change Bill1 has already passed the House of Representatives. Climate change is recognised by scientists, public health experts, Indigenous leaders, economists and the Australian public at large as the most pressing issue at our doorstep.2-5 As we consider the veracity of net zero emission election commitments and the architecture of a post-pandemic recovery in Australia, we use science, public health expertise and a common chronic condition to explain the links between key issues and outline a road map for action in Australia. In this commentary, we highlight current evidence on the relationships between climate change, air pollution, fossil fuel use and their associated impacts on public health. We use asthma as a case study to examine the economic and human health burden arising from this climate-air pollution-fossil fuel triad. Australia's dependence on fossil fuels and gaps in energy policy are underscored as drivers of negative climate and public health outcomes. We provide a roadmap for action consisting of a mandate for: rapid de-carbonisation of Australia's energy systems; adoption of a healthcare without harm framework; and preparing public health systems to prevent and control asthma exacerbations. Climate change is the greatest threat to public health of the 21st century.6 The planet has warmed significantly over the past century by on average 0.8°C, largely as a result of increased global emissions of carbon dioxide and other greenhouse gases (GHG).7 Human activity and fossil fuel-based, carbon intensive energy systems have contributed substantially to global heating. Climate change is having profound effects on weather systems, exemplified by the increased frequency and duration of extreme weather events including floods, drought and bushfires. Climate change also adversely impacts on atmospheric air quality and air pollution.1 The relationship between climate change and air quality is bi-directional: climate change can exacerbate or increase existing air pollutants (e.g., atmospheric heating increases ground level ozone); air polluting emissions influence the climate (e.g., release of carbon-based materials such as black soot have a heating effect); several sources of air pollution are sources of GHGs (e.g., methane locks heat in the atmosphere, triggering climate change). Incomplete combustion of fossil fuels is a primary source of air pollutants (e.g., particulate matter [PM]2.5) and is harmful to human health.8 Higher temperatures and carbon dioxide levels arising from climate change also increase airborne allergenic pollens contributing to allergic asthma.9 The energy sector is the largest contributor to GHG emissions in Australia.8 Australia's primary energy consumption is dominated by fossil fuels (i.e., coal 40%, oil 34% and gas 22%)10 and its electricity system is founded on centralised, carbon-intensive coal-fired generation. Australia's coal burning (and exports) contributes to climate change and air pollution and hence health impacts. Every step of coal's lifecycle produces air pollutants that affect human health. Burning coal produces fly ash and particulate matter (PM2.5), which lodge in the lungs, causing irritation and inflammation.11 Transport (energy) is the second largest source of emissions after electricity production.12 The road transport sector, including passenger and commercial vehicles, is reliant on petroleum-based fossil fuels and is a significant contributor to air pollution in cities and regions.13 For example, petrol and diesel emissions arising from road traffic are a major culprit in asthma exacerbations: Nitrogen dioxide (NO2) exposure and living in close proximity to a major road are associated with an increase in the likelihood of asthma in children and adults.14, 15 Asthma is one of the most common and costly of all chronic disease conditions affecting more than 260 million people globally, and both its prevalence and incidence is strongly associated with air quality and atmospheric pollution16 In 2021, 2.7 million people (10.7%) of the Australian population had asthma, making it a common non-communicable disease17 and accounting for 417 deaths in 2020.18 Nationally, there were over 37 000 hospitalisations with asthma as the principal diagnosis in 2016 and around 2% of all general practitioner encounters were for asthma, representing the 14th most common reason for a general practitioner consultation in that year.19, 20 As asthma is a lifelong condition, the costs associated with the condition are high, both to the individual as well as to the health service, where it accounts for $770 million in direct expenditures annually.19 Studies of coal mine fires and coal town residency illuminate the fossil fuel, air pollution and asthma relationship. The Hazelwood coal mine fire in the Latrobe Valley, Victoria in 2014 created plumes of smoke and ash with high PM2.5 for 45 days. Guo et al.21 found increased risks of all-causes, respiratory diseases, and asthma related emergency presentations and hospital admissions. Casey et al.11 found living near coal-fired power plants is linked to higher rates of respiratory disease and increased asthma exacerbations, while shutting down a coal plant or upgrading emission controls decreases inhaler use, emergency department visits and hospitalisation for asthma among local residents. Gas has also been associated with childhood asthma: one study of Australian children reported the population attributable fraction for childhood asthma associated with household gas stoves (which release PM2.5, NO2) for childhood asthma was approximately 12%, corresponding to over 2700 disability adjusted life years.15 Climate change is increasing the frequency and intensity of bushfires in Australia. Smoke from bushfires is a major risk factor for asthma exacerbations: the 2019–2020 summer bushfires have been linked to 429 premature deaths, more than 2000 hospitalisations for respiratory health issues and 1500 emergency department presentations with asthma.235 The health-related economic costs of the 2019–2020 bushfires was estimated AU$1.95 billion, with the majority due to the economic costs of premature mortality associated with the bushfires; AU$25 million of healthcare costs, $24 million for cardiovascular and respiratory hospitalisations, and AU$1 million for asthma emergency department attendances.22 Climate change effects allergic diseases.23 Thunderstorm asthma is an allergic asthma response to airborne allergenic pollens that rupture due to osmotic shock following a thunderstorm event, and thereby allowing smaller allergenic sub-pollen particles to reach the lower airways to trigger the potentially deadly allergic response24 (see Figure 1). In November 2016, the phenomenon of thunderstorm asthma caused 10 deaths in Australia and more than 3300 ED presentations.19, 24 Several studies have shown that plants growing in highly polluted air produce more allergenic pollen.25 When combined with pollen rupture, it results in a volatile mix that turns such pollens into ‘biological time bombs’. Knox et al.26 have shown that the major allergen of rye grass pollen has the capacity to directly interact with diesel exhaust carbon particles (DECP). They assert allergen-loaded DECP has the capacity to penetrate the lower airways and prompt an episode of asthma. Figure 1 describes the relationship between air pollution, climate change, fossil fuels and thunderstorm asthma as a public health issue. Healthcare—one of the world's largest industries—contributes to climate change and air pollution. The Australian healthcare system is responsible for ~7% of national GHGs.27 In the United States, one study has estimated that healthcare-related air pollution was responsible for 9% of respiratory disease burden from PM emissions.28 Similar estimates of disease impact are not available locally, but Australian healthcare is responsible for around 3% of national PM footprint.29 Paradoxically, some asthma treatments are significant contributors to GHGs. Metered-dose inhalers for asthma contribute an estimated 3.9% of the total carbon footprint of the UK National Health Service,30 due to the extremely potent GHGs used as propellants in some delivery systems. Australian estimates are not available, but the same products are widely used in this country. This scenario demonstrates perverse feedback loops—air pollution and climate change drive each other, and both drive increasing asthma incidence through various pathways, while treating asthma can itself further drive climate change through GHG emissions. This is a critical decade. Linear, single issue and reductionist approaches will not cut through the complex public health challenges arising from the climate change, air pollution and fossil fuel triad. Here we offer the new federal government and health sector a three-point roadmap for action. The roadmap highlights key public health-oriented interventions, which will prevent health-harming emissions, promote a healthy recovery from the pandemic and help Australians prepare for increasing asthma prevalence due to environmental triggers. Australia remains heavily dependent on fossil fuels and is unlikely to keep its commitments to the Paris Agreement to which it is a signatory. Since 1990, there has only been a 10% reduction in the share of electricity generation produced from non-renewable fuels (89.9% in 1990 to 80.2% in 2019) with more than half of total generation still reliant on coal.31 Stopping fossil fuel development and decarbonising energy systems are the most urgent and far reaching challenges of this decade.32 To prevent health harming air polluting emissions and to meet the goals of the Paris Agreement, Australia requires a coherent and timely policy framework that enables disinvestment in fossil fuels and a rapid transition to renewable energy. Central to this policy framework are climate change mitigation targets—an essential upstream and long-term public health strategy for managing the underlying causes of the increasing bushfire risk and thunderstorm asthma. This critical, foundational government policy framework will also support emission reduction efforts within the Australian healthcare sector.33 Action must be taken now, as limiting global heating to 1.5°C will require deep emissions reductions of at least 45% from 2010 levels by 2030.7 Australia's healthcare sector needs to reduce its total emissions to net zero. By 2030, an 80% reduction in emissions is required for healthcare to help meet the 1.5°C Paris Agreement commitments and minimise the predicted catastrophic public health consequences of climate change.33, 34 Australian hospitals and health systems must implement interventions which will decarbonize healthcare delivery to ‘first do no harm’ whilst maintaining and improving health. Healthcare systems can take cost-effective action to transition toward zero emissions energy, buildings, travel and transport, waste management as well as low emissions pharmaceuticals, sustainable food system ectera.35 There are multiple health service level examples of successful action (see Global Green and Health Hospitals36) and state and territory government policy leadership can support compliance and implementation. Substitution of high emission products with more climate friendly alternatives and incentivising the production of green medications is another key strategy. This is particularly relevant to asthma medication. Alternative delivery mechanisms to metered dose inhalers without the high global heating potential propellants, such as dry powder based inhalers, are available and suitable for the majority of patients.35 Wilkinson et al.30 study found that switching to low global warming potential asthma inhalers has co-benefits for reducing GHGs and drug costs. Many peak health and medical bodies have declared a climate emergency. We support the call by Australia's peak associations including Doctors for the Environment Australia, Australian Medical Association, Royal Australian College of Physicians and the Climate and Health Alliance for the establishment of an Australian Sustainable Healthcare Unit to lead and coordinate initiatives and collaboration nationwide.33 Australia's recent bushfire smoke-related and thunderstorm asthma epidemics were climate change and air pollution driven disasters of national and/or state level significance. Both events tested public health system preparedness and responsiveness and capacity to prevent and control environmental health hazards. We support the Royal Commission into National Natural Disaster Arrangement's recommendations, specifically those pertaining to community education, air quality and health.37 Further, we endorse Vardoulakis et al.'s38 perspective that consistency of air quality information and related public health advice across jurisdictions in Australia is essential. We support their call for an independent national expert committee on air pollution and health protection to be established to support environmental health decision making in Australia. Likewise, the impact of climate change (longer pollen seasons, more extreme weather events) on asthma prevalence and severity needs to prioritised in public health planning and surveillance efforts. Notably, the current National Asthma Strategy (2018) is mute on climate change and air pollution. Australians voted for action on climate change in the 2022 federal election. The evidence is clear, we need rapid transition from fossil fuel toward renewable-energy powered systems, including net zero healthcare systems, which will provide benefits for public health, climate and economy. Yet, it remains to be seen whether the pace of change envisaged in the Climate Change Bill 2022 is sufficiently fast, or whether new coal and gas generation and mining projects will be phased out. Continued failure to rapidly act on the climate-air pollution-fossil fuel triad in Australia is likely to result in increased asthma prevalence and severity and exert an inexorable toll on the health, social and economic wellbeing of future generations. Asthma is just the tip of the iceberg. Health and medical groups have a key role in helping chart a new course with the incoming federal government to avert the cascading impacts of this ubiquitous climate-driven public health crisis. Open access publishing facilitated by Deakin University, as part of the Wiley - Deakin University agreement via the Council of Australian University Librarians. None. The authors declare no conflicts of interest except Rebecca Patrick. Data sharing not applicable to this article as no datasets were generated or analysed during the current study.

Ocular allergy is an immunoglobulin E-mediated Type I hypersensitivity reaction localised to the ocular surface and surrounding tissues. Primary signs and symptoms of ocular allergy include itching, redness, irritation and inflammation. Eye-rubbing caused by itching has been shown to alter ocular surface protein concentrations in conditions linked to ocular allergy such as keratoconus. In keratoconus, the cornea begins to thin and sag over time, leading to progressive vision loss and blindness in severe conditions. Due to the high incidence of ocular allergy sufferers rubbing their eyes in response to symptoms of itching, the protein landscape of the ocular surface may be significantly altered. Differential protein expression caused by long-term inflammation and eye-rubbing may lead to subsequent changes in ocular surface structure and function over time. This review aims to summarise and explore the findings of current ocular allergy proteome research conducted using techniques such as gel electrophoresis, mass spectrometry and lab-on-a-chip proteomics. Proteins of interest for this review include differentially expressed immunoglobulins, mucins, functional proteins, enzymes and proteins with previously uncharacterised roles in ocular allergy. Additionally, potential applications of this research are addressed in terms of diagnostics, drug development and future research prospects.

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.