Stacy Soh1, Liat Hui Loo2, Natasha Jamali3, Matthias Maiwald4, Joel Aik5. 1. Environmental Epidemiology and Toxicology Division, National Environment Agency, 40 Scotts Road, Environment Building, #13-00, 228231, Singapore. Electronic address: stacy_soh@nea.gov.sg. 2. Department of Pathology and Laboratory Medicine, KK Women's and Children's Hospital, 100 Bukit Timah Road, 229899, Singapore; Duke-NUS Graduate Medical School, 8 College Road, 169857, Singapore. Electronic address: loo.liat.hui@kkh.com.sg. 3. Environmental Monitoring and Modelling Division, National Environment Agency, 40 Scotts Road, #13-00, 228231, Singapore. Electronic address: Natasha_Jamali@nea.gov.sg. 4. Department of Pathology and Laboratory Medicine, KK Women's and Children's Hospital, 100 Bukit Timah Road, 229899, Singapore; Duke-NUS Graduate Medical School, 8 College Road, 169857, Singapore; Department of Microbiology and Immunology, Yong Loo Lin School of Medicine, NUHS Tower Block, 1E Kent Ridge Road Level 11, 119228, Singapore. Electronic address: matthias.maiwald@singhealth.com.sg. 5. Environmental Epidemiology and Toxicology Division, National Environment Agency, 40 Scotts Road, Environment Building, #13-00, 228231, Singapore; Pre-Hospital & Emergency Research Centre, Duke-NUS Medical School, 8 College Road, 169857, Singapore. Electronic address: joel_aik@nea.gov.sg.
Abstract
OBJECTIVES: Evidence of the relationship between climate variability, air pollution and human parainfluenza virus (HPIV) infections has been inconsistent. We assessed this in a paediatric population from a highly urbanized tropical city-state. METHODS: We analysed all reports of HPIV infections in children <5 years old obtained from a major specialist women and children's hospital in Singapore. Assuming a negative binomial distribution and using multivariable fractional polynomial modelling, we examined the relations between climate variability, air quality and the risk of HPIV infections, adjusting for time-varying confounders. RESULTS: We identified 6393 laboratory-confirmed HPIV infections from 2009 to 2019. Every 1 °C decline in temperature was associated with a 5.8% increase (RR: 0.943, 95% Confidence Interval [95% CI]: 0.903-0.984) in HPIV infection risk 6 days later. Every 10% decrease in relative humidity was associated with a 15.8% cumulative increase in HPIV risk over the next 6 days (cumulative RR: 0.842, 95% CI: 0.771-0.919). Rainfall was positively associated with HPIV risk 2 days later (RR: 1.021, 95% CI: 1.000-1.043). A within-year seasonal rise of HPIV was driven by HPIV-3 and HPIV-1 and preceded by a seasonal decline in temperature. Gender was an effect modifier of the climate-HPIV relationship. Air quality was not associated with HPIV risk. CONCLUSIONS: This study demonstrates a close association between HPIV infection risk and tropical climate variability. The climate dependence and seasonal predictability of HPIV can inform the timing of community campaigns aimed at reducing infection risk and the development of hospital resources and climate adaption plans.
OBJECTIVES: Evidence of the relationship between climate variability, air pollution and human parainfluenza virus (HPIV) infections has been inconsistent. We assessed this in a paediatric population from a highly urbanized tropical city-state. METHODS: We analysed all reports of HPIV infections in children <5 years old obtained from a major specialist women and children's hospital in Singapore. Assuming a negative binomial distribution and using multivariable fractional polynomial modelling, we examined the relations between climate variability, air quality and the risk of HPIV infections, adjusting for time-varying confounders. RESULTS: We identified 6393 laboratory-confirmed HPIV infections from 2009 to 2019. Every 1 °C decline in temperature was associated with a 5.8% increase (RR: 0.943, 95% Confidence Interval [95% CI]: 0.903-0.984) in HPIV infection risk 6 days later. Every 10% decrease in relative humidity was associated with a 15.8% cumulative increase in HPIV risk over the next 6 days (cumulative RR: 0.842, 95% CI: 0.771-0.919). Rainfall was positively associated with HPIV risk 2 days later (RR: 1.021, 95% CI: 1.000-1.043). A within-year seasonal rise of HPIV was driven by HPIV-3 and HPIV-1 and preceded by a seasonal decline in temperature. Gender was an effect modifier of the climate-HPIV relationship. Air quality was not associated with HPIV risk. CONCLUSIONS: This study demonstrates a close association between HPIV infection risk and tropical climate variability. The climate dependence and seasonal predictability of HPIV can inform the timing of community campaigns aimed at reducing infection risk and the development of hospital resources and climate adaption plans.