Ambient Air Pollutant Exposures and Hospitalization for Kawasaki Disease in Taiwan: A Case-Crossover Study
Chau-Ren Jung1, Wei-Ting Chen, Yu-Ting Lin
1Department of Occupational Safety and Health, College of Public Health, China Medical University, Taichung, Taiwan.
Background:
Kawasaki disease (KD) is an acute and multi-systemic vasculitis that occurs predominantly in infants and young children. Although the etiological agent of KD remains unclear, limited studies have reported that windborne environmental factors may trigger KD.
Objectives:
We conducted a time-stratified case-crossover study to assess the associations between air pollutants and KD in Taiwan.
Methods:
We identified children < 5 years old with a diagnosis of KD from the Longitudinal Health Insurance Database 2000 (LHID2000) between 2000 and 2010. We obtained data regarding carbon monoxide (CO), nitrogen dioxide (NO2), ozone (O3), particulate matter with aerodynamic diameter < 10 μm (PM10), and sulfate dioxide (SO2) from 70 monitoring stations and used inverse distance weighting to calculate average daily exposures for the residential postal code of each case. We performed conditional logistic regression to estimate associations between KD and each air pollutant according to interquartile range (IQR) increases and quartiles of exposure on the day of hospitalization versus 3-4 reference days during the same month for each case. Additionally, we estimated associations with single-day exposures lagged 1-2 days.
Results:
We identified 695 KD hospital admissions during the study period. An IQR increase (28.73 ppb) of O3 was positively associated with KD after adjusting for temperature, humidity, northward wind, and eastward wind [adjusted odds ratio = 1.21; 95% confidence interval (CI): 1.01, 1.44]. There were no significant associations between KD and CO, NO2, PM10, or SO2. The association with O3 was limited to exposure on the day of hospitalization and to exposure during the summer months (June-August).
Conclusions:
Our results provide new evidence that exposure to O3 may increase the risk of KD in children. However, further investigation is needed to confirm the association and identify a potential biological mechanism.
