Objectives High ambient temperatures may contribute to acute asthma exacerbation, a leading cause of morbidity in children. We quantified associations between hot-season ambient temperatures and asthma exacerbation in children ages 0–18 years in Philadelphia, PA.
Methods We created a time series of daily counts of clinical encounters for asthma exacerbation at the Children’s Hospital of Philadelphia linked with daily meteorological data, June–August of 2011–2016. We estimated associations between mean daily temperature (up to a 5-day lag) and asthma exacerbation using generalised quasi-Poisson distributed models, adjusted for seasonal and long-term trends, day of the week, mean relative humidity,and US holiday. In secondary analyses, we ran models with adjustment for aeroallergens, air pollutants and respiratory virus counts. We quantified overall associations, and estimates stratified by encounter location (outpatient, emergency department, inpatient), sociodemographics and comorbidities.
Results The analysis included 7637 asthma exacerbation events. High mean daily temperatures that occurred 5 days before the index date were associated with higher rates of exacerbation (rate ratio (RR) comparing 33°C–13.1°C days: 1.37, 95% CI 1.04 to 1.82). Associations were most substantial for children ages 2 to <5 years and for Hispanic and non-Hispanic black children. Adjustment for air pollutants, aeroallergens and respiratory virus counts did not substantially change RR estimates.
Conclusions This research contributes to evidence that ambient heat is associated with higher rates of asthma exacerbation in children. Further work is needed to explore the mechanisms underlying these associations.
- public health
- environmental pollution
Data availability statement
No data are available. The data used for this study are not permitted for reuse due to confidentiality concerns.
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Contributors LHS conceived of the study, assisted with data preparation, and led data analysis and manuscript writing.CK contributed to study design and manuscript writing. RAH contributed to results interpretation and manuscript writing. YZ contributed to data preparation. MM contributed to data preparation. SJM contributed to data preparation and manuscript writing. KM contributed to data preparation and manuscript writing. CBF contributed to project funding acquisition and manuscript writing. AVDR contributed to project funding acquisition and manuscript writing. AJdR contributed to data preparation, project conception, analysis interpretation and planning, and manuscript writing. As guarantor, LHS takes responsibility for the overall content of this work.
Funding This work was supported by a grant from the Commonwealth Universal Research Enhancement (C.U.R.E) programme funded by the Pennsylvania Department of Health—2015 Formula award—SAP #4100072543.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.
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