OBJECTIVES: To determine the effects of the January 1994 Sydney bushfire on evening peak expiratory flow rates (PEFR) in children with wheeze. METHODS: Children with a history of wheeze were enrolled in the longitudinal study and completed a daily asthma diary. We obtained daily air pollution, meteorological, pollen and alternaria data. We then used generalised estimating equation techniques to determine associations between the bushfire period and particulate matter less than 10 microns (PM10) and PEFR. RESULTS: The maximum daily PM10 level peaked at 210 ug/m3, which was nearly seven times the usual PM10 level for the rest of January and February 1994. There was no significant association between mean PM10 and PEFR (beta-coefficient = -0.009, p = 0.86). Children without bronchial hyper-reactivity had a significant negative association between PEFR and PM10 (beta-coefficient = -0.1029, p = 0.03). The bushfire period was not significant in any of the models. CONCLUSIONS: We did not find an association between the bushfire period or PM10 and evening PEFR, although in a subgroup of children without bronchial hyper-reactivity, a significant negative association was present between PM10 and evening PEFR. IMPLICATIONS: We conclude that the high levels of particulate pollution caused by the Sydney bushfires did not lead to any clinically significant reductions in PEFR in symptomatic children. Our results have implications for community risk communication during future bushfires.
OBJECTIVES: To determine the effects of the January 1994 Sydney bushfire on evening peak expiratory flow rates (PEFR) in children with wheeze. METHODS:Children with a history of wheeze were enrolled in the longitudinal study and completed a daily asthma diary. We obtained daily air pollution, meteorological, pollen and alternaria data. We then used generalised estimating equation techniques to determine associations between the bushfire period and particulate matter less than 10 microns (PM10) and PEFR. RESULTS: The maximum daily PM10 level peaked at 210 ug/m3, which was nearly seven times the usual PM10 level for the rest of January and February 1994. There was no significant association between mean PM10 and PEFR (beta-coefficient = -0.009, p = 0.86). Children without bronchial hyper-reactivity had a significant negative association between PEFR and PM10 (beta-coefficient = -0.1029, p = 0.03). The bushfire period was not significant in any of the models. CONCLUSIONS: We did not find an association between the bushfire period or PM10 and evening PEFR, although in a subgroup of children without bronchial hyper-reactivity, a significant negative association was present between PM10 and evening PEFR. IMPLICATIONS: We conclude that the high levels of particulate pollution caused by the Sydney bushfires did not lead to any clinically significant reductions in PEFR in symptomatic children. Our results have implications for community risk communication during future bushfires.
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