Prenatal and early life exposure to air pollution and the incidence of Kawasaki disease

Abstract

AbstractKawasaki disease (KD) is the most common form of acquired pediatric cardiac disease in the developed world. However, its etiology is still unclear. Epidemiological studies have shown that air pollution is a plausible risk factor in stimulating oxidative stress, inducing inflammation and causing autoimmune diseases. This study aims to assess the connections between prenatal and early life air pollution exposure to the incidence of KD. The main data source of this nationwide longitudinal study was the National Health Insurance Research Database (NHIRD) of Taiwan. NHIRD was linked with Taiwan Maternal and Child Health Database to establish the link between mothers and children. In total, 4192 KD cases involving children under 6 years of age were identified between January 2004 and December 2010. Children in the control group were randomly selected at a 1:4 ratio and matched using their age and index year. Integrated data for the air pollutants were obtained from 71 Environmental Protection Agency monitoring stations across Taiwan. Patients who had main admission diagnosis of KD and subsequently received intravenous immunoglobulin treatment were defined as incidence cases. Ambient exposure, including pollutant standards index (PSI), carbon monoxide (CO), nitric oxide (NO), nitric dioxide (NO2), and nitrogen oxide (NOx) during pregnancy were all positively associated with KD incidence. Conversely, ozone (O3) exposure had a negative correlation. Exposure to CO, NO, NO2, and NOx after childbirth remained consistent with regards to having a positive association with KD incidence. Exposure to PSI and O3 after delivery displayed no significant association with KD. Both prenatal and postnatal cumulative CO, NO, NO2, and NOx exposure had a dose dependent effect towards increasing KD incidence. Certain prenatal and early life air pollutant exposure may increase the incidence of KD.