Melbourne School of Population and Global Health - Theses
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ItemThe role of short-term grass pollen exposure in allergic disease and lung health( 2023-02)Background: Australia has one of the highest prevalence of allergic diseases. Although the mortality rate is low, allergic conditions are associated with significant burden. Environmental risk factors of allergic diseases include exposure to aeroallergens such as pollen. In Australia, temperate grass pollen is the primary seasonal aeroallergen. Research Gaps: Although it is well-established that temperate grass pollen can trigger asthma hospitalisations, its relationship with lung function and airway inflammation at a community level is understudied. Furthermore, no study to date has considered the short-term associations between pollen exposure and food allergy. Studies on selective populations have shown that eczema can be exacerbated with increasing ambient pollen exposure, but population-based studies are lacking. Moreover, the evidence on the potential effect modification by individual and environmental factors on the associations is scarce. Aim: I investigated the associations between short-term grass pollen exposure and lung function, airway inflammation, food allergy and eczema across different age groups within the community and identified potential effect modifiers of these associations. Methods: My doctoral research utilised a systematic review methodology and original data from large population-based cohorts: HealthNuts, The Melbourne Atopy Cohort Study (MACS) and the Tasmanian Longitudinal Health Study (TAHS). Grass pollen exposure was assessed either using daily concentrations or the season as a proxy measure of exposure. Where daily pollen data were available, exposure was investigated on the day of exposure (lag 0) and up to three days before (lag 3). Statistical modelling was performed accounting for the distribution of the model residuals, the functional form for the associations between the exposure and outcomes, and confounders. Interactions with individual and environmental factors were explored using likelihood ratio tests. Results: Research Question 1 – The systematic review showed that outdoor pollen exposure is an important risk factor for type-2 inflammation in the upper and lower airways in people with ever asthma and/or seasonal allergic rhinitis, but the evidence on lung function was limited (Chapter 3). Research Question 2 – Increasing grass pollen concentrations were associated with reversible obstructive lung function deficits in children with allergic disease, the greatest risk of exacerbation in food allergic children (Chapter 5). Research Question 3 – There was evidence of a relationship between increasing grass pollen concentrations, and subsequent airway inflammation (1-2 days after the exposure) and lung function deficits (2-3 days after the exposure). Adults and individuals with co-existing allergic diseases were especially vulnerable. (Chapter 6). Research Question 4 – Peak grass pollen season was associated with lower pre- and post-bronchodilator lung function in smokers with allergic respiratory disease, those exposed to higher traffic-related air pollution, with co-existing allergic diseases or with poor adherence to inhaled corticosteroids (Chapter 7). Research Question 5 – Persistent grass pollen exposure over 4 days was associated with increased odds of food skin-prick test reactivity and eczema flares in children, but the impact was greater if peanut allergy was already present (Chapter 8). Conclusions: My work has significant public health and clinical implications. Notably, there was evidence of association between ambient grass pollen exposure, and subsequent lung function impairment and airway inflammation in both children and adults, mainly on the large and medium-small sized airways. There was also an association with post-bronchodilator measures in middle-aged adults, implying that the pathology in this age group may be distinct from classic, reversible asthma. Furthermore, the negative health impacts of short-term grass pollen exposure may extend to non-respiratory allergic diseases such as food allergy and eczema. Lastly, I identified high-risk groups who were more vulnerable to grass pollen, which were adults, smokers with allergic respiratory disease, those exposed to higher traffic-related air pollution, with allergic co-morbidities or with poor adherence to inhaled corticosteroids.
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ItemThe contribution of outdoor fungal spores to child and adolescent asthma hospitalisations: lung function and airway inflammation( 2017)Outdoor fungal spores are among the most common aerobiological particles in the air we breathe. Although a limited number of outdoor fungal species are recognised as exacerbating agents of a number of allergic and respiratory conditions, their contribution towards asthma exacerbation is unclear, particularly among children and adolescents. Moreover, we have limited understanding of the impacts that inhaled fungal spores have on lung function or airway inflammation, which may be pre-clinical signs of asthma exacerbation. Therefore the aim of my doctoral research is to examine whether there are associations between common outdoor fungal spores and child and adolescent asthma hospitalisations, and also to explore if short term exposure to ambient fungal spores is associated with lower lung function or airway inflammation. In Chapter 2, a comprehensive literature review highlights that there are significant knowledge gaps in the contribution of outdoor fungal spores to child and adolescent asthma hospitalisations, lung function and airway inflammation. In order to address some of these gaps, my specific research objectives of this doctoral research were to: (a) systematically synthesise the current evidence as to whether outdoor fungal spores were significant triggers of child and adolescent asthma exacerbations resulting in health service attendances; (b) investigate if there were associations between short term exposure to outdoor fungal spores and child and adolescent asthma hospitalisations; (c) explore if any of these associations were modified by air pollutants, grass pollen, age group, sex, presence of human rhinovirus infection, or fungal sensitisation status; (d) investigate if there were associations between outdoor fungal spores and lower lung function or airway inflammation, and (e) explore if any associations were modified by air pollutants or pollen, age group or fungal sensitisation status. In Chapter 3, my systematic review found that only a small number of studies have been conducted, predominantly in countries located in the northern hemisphere. Children with fungal sensitisation appeared to be at greater risk of asthma hospitalisations. Severity of asthma exacerbation may vary between fungal spore taxa. There were inconsistent findings, possibly due to the lack of accounting for other significant triggers of asthma exacerbations. In Chapter 5, my ecological case-crossover study of child and adolescent asthma hospitalisations in south-west Sydney found that there were associations with Coprinus, Periconia, Chaetomium, Ganoderma and Cerebella, with same day and lagged effects. There was evidence of effect modification by sex, with girls demonstrating stronger associations with Cladosporium, Coprinus and Chaetomium than boys. Age also acted as an effect modifier with older adolescents, demonstrating stronger associations with Coprinus and Ustilago/smuts than those aged under 14 years. In Chapter 6, my case-crossover study of child and adolescent asthma hospitalisations in Melbourne found associations between ambient Alternaria, Coprinus, Drechslera and Leptosphaeria, with signs of same day and lagged effects. These associations were independent of having a human rhinovirus respiratory infection. There was some evidence that Cladosporium sensitisation acted as an effect modifier. In Chapter 7, my cross-sectional study of a high allergy risk cohort comprising of children, adolescents and adults found differing associations between outdoor fungal spores and lower lung function and presence of airway inflammation. Fungal sensitisation acted as an effect modifier with some fungi and parameters of lung function and markers of airway inflammations. Overall, this research has contributed to filling some of the gaps in our current understanding of the contribution of outdoor fungal spore exposures to child and adolescent asthma hospitalisations, lower levels of lung function and airway inflammation. This research demonstrates that the contribution of outdoor fungal spores may be under-estimated. Importantly, species that have not been previously found to be associated with asthma exacerbations, but are genetically related to well-known fungal triggers of asthma exacerbation, may warrant further investigation. Future research needs to improve the modelling of dispersion and distribution of outdoor fungal spores on spatial and temporal levels. The development of reliable and standardised fungal reagents for detection of allergic sensitisation is needed. The presence of fungal spores in the air is important for the ecosystem, and may not be controlled on a large scale, but understanding how to prevent their effects on respiratory health will benefit public health.