Environmental Tobacco Smoke Exposure in Relation to Attention-deficit/Hyperactivity Disorder and Learning Disabilities in School-aged Children

Abstract

PP-31-061 Background/Aims: The aim of this study was to examine the relationship between environmental tobacco smoke exposure, attention-deficit hyperactivity disorder (ADHD), and learning disabilities in school-aged children. Methods: Between 2008 and 2009, the current study enrolled 1089 children (571 boys, 518 girls; range, 8–11 years; mean age = 9.05 ± 0.70 years) in 5 South Korean cities. Urine cotinine was used as a biomarker for environmental tobacco smoke exposure. A cross-sectional examination of urine cotinine levels was performed, and scores on continuous performance test (CPT) were obtained from the children. The parents completed the Korean versions of ADHD Rating Scale-IV and Learning Disability Evaluation Scale. The intelligence quotients of the participating children and their mothers were determined as well. The associations between the urine cotinine concentrations, neuropsychological variables, symptoms of ADHD, and learning disabilities were assessed using linear regression analysis. The cotinine concentration was log transformed (ln) to achieve normal distributions of the variables. Path analyses were conducted with AMOS 5.0 to determine the best fitting model. Results: After adjusting for demographic and developmental covariates, multiple linear regression analysis showed that urinary cotinine levels were significantly and positively associated with the scores of omission errors, commission errors, and response time variability of the CPT (P < 0.01). The path analysis model revealed that the association between urine cotinine levels and parental reports on symptoms of ADHD and learning disabilities was mediated by the neuropsychological variables of the CPT. The proposed model showed an excellent fit to the data (RMSEA = 0.038, NFI = 0.986, CFI = 0.991). Conclusion: Our data suggest that environmental exposure to tobacco smoke might be a contributor to ADHD and learning disabilities in children, and that its effects seem to be mediated by neuropsychological impairments.