Rachel Tham1, Constance H Katelaris2, Don Vicendese3, Shyamali C Dharmage4, Adrian J Lowe5, Gayan Bowatte6, Philip Taylor7, Pamela Burton8, Michael J Abramson9, Bircan Erbas10. 1. Allergy and Lung Health Unit, Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, University of Melbourne, Melbourne, Victoria, Australia. Electronic address: rtham@student.unimelb.edu.au. 2. Western Sydney University, Department of Medicine, Immunology and Allergy, Campbelltown Hospital, Campbelltown, New South Wales, Australia. Electronic address: connie.katelaris@sswahs.nsw.gov.au. 3. School of Public Health, College of Science Health and Engineering, La Trobe University, Bundoora, Victoria, Australia. Electronic address: vicendese.don@gmail.com. 4. Allergy and Lung Health Unit, Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, University of Melbourne, Melbourne, Victoria, Australia. Electronic address: s.dharmage@unimelb.edu.au. 5. Allergy and Lung Health Unit, Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, University of Melbourne, Melbourne, Victoria, Australia. Electronic address: lowea@unimelb.edu.au. 6. Allergy and Lung Health Unit, Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, University of Melbourne, Melbourne, Victoria, Australia. Electronic address: gbowatte@gmail.com. 7. School of Life and Environmental Sciences, Deakin University, Geelong, Victoria, Australia. Electronic address: philip.taylor@deakin.edu.au. 8. Western Sydney University, Department of Medicine, Immunology and Allergy, Campbelltown Hospital, Campbelltown, New South Wales, Australia. Electronic address: Pamela.Burton@sswahs.nsw.gov.au. 9. Department of Epidemiology and Preventive Medicine, School of Public Health and Preventive Medicine, Monash University, Melbourne, Victoria, Australia. Electronic address: michael.abramson@monash.edu. 10. School of Public Health, College of Science Health and Engineering, La Trobe University, Bundoora, Victoria, Australia. Electronic address: B.Erbas@latrobe.edu.au.
Abstract
BACKGROUND: Some fungal spores can trigger asthma exacerbation but knowledge of which outdoor fungal spores contribute to asthma hospitalisation is limited. OBJECTIVES: To examine the role of outdoor fungal spores in child and adolescent asthma hospitalisations. METHODS: We conducted a bi-directional time-stratified case-crossover study of child and adolescent asthma hospitalisations over 5 years. Conditional logistic regression assessed the role of 20 fungi taxa (Same day [L0] and lagged [L1-3]) adjusted for maximum temperature, humidity and grass pollen. Strata specific effects were explored if there was evidence of effect modification by age, sex, air pollutants or grass pollen. Non-linear effects examined with Generalized Additive Models. RESULTS: Of 2098 children hospitalised for asthma, 60% were boys; mean age was 5.5±3.7 years. Fungal spore counts peaked during warm months. Regression models found weak associations with Coprinus [L0,L1: OR=1.03, 1.01-1.06], Periconia [L0: OR=1.03, 1.001-1.07] and Chaetomium [L2: OR=1.08, 1.0-1.2]. Sex appeared to act as an effect modifier with girls having stronger associations with Cladosporium, Coprinus and total fungi. Older adolescent (14-18 years) hospitalisation was significantly associated with Coprinus and Ustilago/smuts. Air pollutants and grass pollen did not appear to act as effect modifiers. Non-linearity was not detected. CONCLUSION: There may be associations between some outdoor fungal spores and asthma hospitalisations. Further research needed to explore whether these findings can be replicated; and examine whether fungal sensitisation and/or human rhinovirus infections are associated with stronger effects. If findings are replicated, then the need to develop predictive models for fungal spore distribution and levels may become more important.
BACKGROUND: Some fungal spores can trigger asthma exacerbation but knowledge of which outdoor fungal spores contribute to asthma hospitalisation is limited. OBJECTIVES: To examine the role of outdoor fungal spores in child and adolescent asthma hospitalisations. METHODS: We conducted a bi-directional time-stratified case-crossover study of child and adolescent asthma hospitalisations over 5 years. Conditional logistic regression assessed the role of 20 fungi taxa (Same day [L0] and lagged [L1-3]) adjusted for maximum temperature, humidity and grass pollen. Strata specific effects were explored if there was evidence of effect modification by age, sex, air pollutants or grass pollen. Non-linear effects examined with Generalized Additive Models. RESULTS: Of 2098 children hospitalised for asthma, 60% were boys; mean age was 5.5±3.7 years. Fungal spore counts peaked during warm months. Regression models found weak associations with Coprinus [L0,L1: OR=1.03, 1.01-1.06], Periconia [L0: OR=1.03, 1.001-1.07] and Chaetomium [L2: OR=1.08, 1.0-1.2]. Sex appeared to act as an effect modifier with girls having stronger associations with Cladosporium, Coprinus and total fungi. Older adolescent (14-18 years) hospitalisation was significantly associated with Coprinus and Ustilago/smuts. Air pollutants and grass pollen did not appear to act as effect modifiers. Non-linearity was not detected. CONCLUSION: There may be associations between some outdoor fungal spores and asthma hospitalisations. Further research needed to explore whether these findings can be replicated; and examine whether fungal sensitisation and/or human rhinovirus infections are associated with stronger effects. If findings are replicated, then the need to develop predictive models for fungal spore distribution and levels may become more important.
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