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Asthma is a common but complex heterogenous inflammatory airway disorder. Despite significant developments in our understanding of the pathophysiology and treatment of asthma, it remains a major cause of mortality and morbidity. Optimal management involves addressing modifiable risk factors, titration of inhaled pharmacotherapy in a stepwise approach and, in severe disease, consideration of biologic agents. Appreciation of the clinical characteristics of asthma and recognition of the immune pathways involved has allowed the development of phenotypic and endotypic subtypes of asthma to be better defined. This has revolutionised asthma management, allowing risk stratification of patients, targeted use of biologic agents to modify cytokine responses that drive asthma and improved patient outcomes. Patient education and engagement are critical to the management of this disease in an era of personalised medicine and a rapidly changing global environment. [ABSTRACT FROM AUTHOR]

Over recent years, Australians have been subject to an unprecedented number of environmental events materially and visibly affecting air quality, including thunderstorm asthma and bushfire smoke. There is increasing evidence that poor air quality adversely affects health with consequences for mortality and morbidity with measured particulates (PM2.5) in January 2019 frequently exceeding World Health Organization standards. Biological factors can also impact air quality with thunderstorm asthma epidemics evidence of a prime example, the 2016 event being associated with severe impacts on health services. Given these events, consideration needs to be given to environmental health literacy which will support individuals with pre‐existing illness to recognise and mitigate as far as possible the effects of adverse air quality. Recognising the impact of poor air quality should also urge physicians to advocate for clean air as a necessity for good health. [ABSTRACT FROM AUTHOR]

International studies report marked increases in the prevalence of food allergy, along with increases in hospital admissions and emergency presentations for severe allergic reactions due to foods. The prevalence of self-reported food allergy is common, but generally exceeds that which can be verified from challenge studies, although nut allergies appear to be an important exception to this rule. Studies examining food allergy deaths suggest that those who die of food allergy usually have co-existent asthma. Adolescents and young adults are at most risk, and adrenaline auto-injectors are sub-optimally used. Food chemical sensitivity is very commonly reported but not usually verified by challenge testing. However, the exception to this is sulphite sensitivity, which can elicit reproducible reactions in some. The increasing prevalence of severe food allergies and awareness of its risk in those with asthma demands an especially rigorous approach to the diagnosis and management of co-existent food allergy and asthma, especially in young people who appear to be at most risk from death from severe food allergy. Cite this as: A. Gillman and Jo A. Douglass, Clinical & Experimental Allergy, 2010 (40) 1295–1302. [ABSTRACT FROM AUTHOR]

Background: While the relationship between pollen and respiratory allergies is well‐documented, the role of short‐term pollen exposure in food allergy and eczema flares has not previously been explored. We aimed to investigate these associations in a population‐based sample of children. Methods: We investigated 1‐ (n = 1108) and 6‐year‐old (n = 675) children in the grass pollen season from the HealthNuts cohort. Grass pollen concentrations were considered on the day of testing (lag 0), up to three days before (lag 1‐lag 3) and cumulatively (lag 0–3). Associations between grass pollen and food skin‐prick test reactivity (SPT ≥ 2 mm at age 1 year and ≥ 3 mm at age 6 years), eczema flares, challenge‐confirmed food allergy, reaction threshold to oral food challenges (OFC), and serum food‐specific IgE levels were analyzed using either logistic or quantile regression models. Atopy and family history of allergic disease were considered as potent effect modifiers. Results: Grass pollen at lag 0–3 (every 20 grains/m3 increase) was associated with an up to 1.2‐fold increased odds of food SPT reactivity and eczema flares in 6‐year‐olds. In 1‐year‐olds, the associations were only observed for peanut in those with a family history of food allergy. Increasing grass pollen concentrations were associated with a lower reaction threshold to OFC and higher serum IgE levels in peanut‐allergic 1‐year‐olds only. Conclusion: Increasing grass pollen concentration was associated with increased risk of food SPT reactivity and eczema flares in children. The associations in peanut‐allergic infants may be related to immune activation and/or peanut and grass pollen cross‐reactivity leading to a lower reaction threshold. [ABSTRACT FROM AUTHOR]

The article describes 2 rare skin conditions not reported to be associated with underlying B-cell chronic lymphocytic leukemia (B-CLL) where specific anti-leukemia treatment successfully eradicated skin lesions. The first case is a 69 year old patient presented with recurrent ulcerated lesions in his lower limbs consistent with pyoderman gangrenosum (PG) and the second case is a 46 year old patient presented in 2008 with generalized painful and itchy urticarial lesions triggered by cold.

Three patients were skin test positive to only goat and sheep milk and four to at least one other milk product from buffalo mozzarella, cow's milk or camel milk. We identified seven adults with new-onset IgE-mediated allergy to orally ingested goat milk products Patients used goat milk skincare products prior to developing allergy, and six had atopic dermatitis Competitive inhibition experiments suggested the skincare products led to transcutaneous sensitization and goat milk allergy To the Editor, Milk allergy is one of the most common food allergies in children, but usually resolves in the first years of life.1 Adult-onset milk allergy is rare. [Extracted from the article]

Background: Experimental challenge studies have shown that pollen can have early and delayed effects on the lungs and airways. Here, we qualitatively and quantitatively synthesize the evidence of outdoor pollen exposure on various lung function and airway inflammation markers in community‐based studies. Methods: Four online databases were searched: Medline, Web of Science, CINAHL and Google Scholar. The search strategy included terms relating to both exposure and outcomes. Inclusion criteria were human‐based studies published in English that were representative of the community. Additionally, we only considered cross‐sectional or short‐term longitudinal studies which investigated pollen exposure by levels or season. Study quality assessment was performed using the Newcastle‐Ottawa scale. Meta‐analysis was conducted using random‐effects models. Results: We included 27 of 6551 studies identified from the search. Qualitative synthesis indicated associations between pollen exposure and predominantly type‐2 inflammation in both the upper and lower airways, but little evidence for lung function changes. People with ever asthma and/or seasonal allergic rhinitis (SAR) were at higher risk of such airway inflammation. Meta‐analysis confirmed a positive relationship between pollen season, eosinophilia and eosinophil cationic protein (ECP) in people with ever SAR but the results between studies were highly variable. Heterogeneity was reduced after further subgrouping by age, and the forest plots indicated that eosinophilic airway inflammation to outdoor pollen exposure increased with age. Conclusion: Among people with ever asthma and ever SAR, exposure to increased ambient pollen triggers type‐2 upper and lower airway inflammation rather than a non‐specific or innate inflammation. These findings can lead to the formulation of specific pollen immunotherapy for susceptible individuals. Future research should be directed towards investigating lagged associations and effect modifications using larger and more generalized populations. Systematic review registration: CRD42020146981 (PROSPERO). [ABSTRACT FROM AUTHOR]

Background: The association between grass pollen exposure and early markers of asthma exacerbations such as lung function changes and increase in airway inflammation is limited. We investigated the associations between short‐term grass pollen exposure and lung function and airway inflammation in a community‐based sample, and whether any such associations were modified by current asthma, current hay fever, pollen sensitization, age, and other environmental factors. Methods: Cross‐sectional and short‐term analyses of data from the Melbourne Atopy Cohort Study (MACS) participants (n = 936). Lung function was assessed using spirometry. Airway inflammation was assessed by fractional exhaled nitric oxide (FeNO) and exhaled breath condensate pH and nitrogen oxides (NOx). Daily pollen counts were collected using a volumetric spore trap. The associations were examined by linear regression. Results: Higher ambient levels of grass pollen 2 days before (lag 2) were associated with lower mid‐forced expiratory flow (FEF25%‐75%) and FEV1/FVC ratio (Coef. [95% CI] = −119 [−226, −11] mL/s and −1.0 [−3.0, −0.03] %, respectively) and also 3 days before (lag 3). Increased levels of grass pollen a day before (lag 1) were associated with increased FeNO (4.35 [−0.1, 8.7] ppb) and also at lag 2. Adverse associations between pollen and multiple outcomes were greater in adults with current asthma, hay fever, and pollen sensitization. Conclusion: Grass pollen exposure was associated with eosinophilic airway inflammation 1‐2 days after exposure and airway obstruction 2‐3 days after exposure. Adults and individuals with asthma, hay fever, and pollen sensitization may be at higher risk. [ABSTRACT FROM AUTHOR]

Background: The world's most catastrophic and deadly thunderstorm asthma epidemic struck Melbourne, Australia, on November 21, 2016. Objective: Among thunderstorm‐affected patients presenting to emergency rooms (ERs), we investigated risk factors predicting severe attacks requiring admission to hospital. Methods: Thunderstorm‐affected patients were identified from ER records at the eight major Melbourne health services and interviewed by telephone. Risk factors for hospital admission were analyzed. Results: We interviewed 1435/2248 (64%) of thunderstorm‐affected patients, of whom 164 (11.4%) required hospital admission. Overall, rhinitis was present in 87%, and current asthma was present in 28%. Odds for hospital admission were higher with increasing age (odds ratio 1.010, 95% CI 1.002, 1.019) and among individuals with current asthma (adjusted odds ratio [aOR] 1.87, 95% CI 1.26, 2.78). Prior hospitalization for asthma in the previous 12 months further increased the odds for hospital admission (aOR 3.16, 95% CI 1.63, 6.12). Among patients of Asian ethnicity, the odds for hospital admission were lower than for non‐Asian patients (aOR 0.59, 95% CI 0.38, 0.94), but higher if born in Australia (OR = 5.42, 95% CI 1.56, 18.83). Conclusions: In epidemic thunderstorm asthma patients who presented to the ER, higher odds for hospital admission among patients with known asthma were further amplified by recent asthma admission, highlighting the vulnerability conferred by suboptimal disease control. Odds for hospital admission were lower in Asian patients born overseas, but higher in Asian patients born locally, than in non‐Asian patients; these observations suggest susceptibility to severe thunderstorm asthma may be enhanced by gene‐environment interactions. We examined patients with acute asthma, who presented to Emergency Rooms during the 2016 Melbourne thunderstorm asthma epidemic. Patients with current asthma had higher odds (1.9) for hospital admission, hospitalization for asthma in the prior 12 months further increased the odds by 3.16. Among patients of Asian ethnicity, odds for hospital admission were lower than for non‐Asian patients (0.59), but higher if born in Australia (5.42), suggesting enhanced susceptibility from gene‐environment interactions. [ABSTRACT FROM AUTHOR]

Introduction: Asthma mortality has declined overall because of a range of public health initiatives. In western countries, the majority of asthma deaths now occur in people over the age of 50. The reasons for the poorer response of older age groups to public health asthma initiatives are not known. Objectives: We undertook a study to investigate the disease perspectives of older people with asthma and barriers which may exist and prevent optimal asthma care. Methods: Fifty-five participants (16 male and 39 female) aged over 50 from an inner city, suburban area and a rural region were recruited. Lung function was measured, and questionnaire data on asthma symptoms, knowledge and control, medication use and respiratory health were collected. Participants were also interviewed in-depth, and the quantitative and qualitative data were triangulated. Results: Participants with a duration of asthma for >30 years reported significantly fewer symptoms and better quality of life irrespective of asthma severity, indicating less appreciation of symptoms in those with a long asthma duration. Interviews revealed this was related to previous asthma management strategies when treatment options were limited. Participants with a recent diagnosis sought understanding of asthma and the reason for their illness. Initiatives to improve asthma care in older people need to reflect these findings. Conclusions: Self-management strategies for older people need to be tailored according to the time of disease onset and the duration of disease. Please cite this paper as: Goeman DP, O’Hehir RE, Jenkins C, Scharf SL and Douglass JA. ‘You have to learn to live with it’: a qualitative and quantitative study of older people with asthma. The Clinical Respiratory Journal 2007; 1:99–105. [ABSTRACT FROM AUTHOR]